Return-Path: Received: from web56204.mail.re3.yahoo.com (web56204.mail.re3.yahoo.com [216.252.110.213]) by ns26.routerdog2.com (8.13.1/8.13.1) with SMTP id mAHHfGX0006138 for ; Mon, 17 Nov 2008 12:41:17 -0500 Received: (qmail 91749 invoked by uid 60001); 17 Nov 2008 17:41:16 -0000 DomainKey-Signature: a=rsa-sha1; q=dns; c=nofws; s=s1024; d=yahoo.com; h=X-YMail-OSG:Received:X-Mailer:Date:From:Reply-To:Subject:To:MIME-Version:Content-Type:Message-ID; b=DGy8N/p4qfRZ/6xJwGSerShYTC/3Q4GzaY4aUa3HlDcUcCxSbOMN1uGYdsRX0MJ9CxHrHwyLdUbsZY0Tz0PLkalEdfqV9MPApUn9DhBn7pl6ZB6EmbBMcNG/eci28ImIUbEa5jTEWwwAT62x3E0NP/gxhR5RBIBnLwKB9qq4tm8=; X-YMail-OSG: 0SHfpDgVM1kQutr8qPGIotR1hyQU3E8kc5yCh8iRdF.77yyQUDedj3ZIhdtdYk9NV.Pv26zBpIkgisyCMuSDXnaRQ54PT_HXirV5VMCZ0IrzHypAM0jDywLN.UiQaS0JPgAf5.6BhP09ZNCb9D4pk74h8NF.nSa3GL23fu3eWNmDAdYd3.evyB2XytQEL1ra86ZXS7uKKYuo_YktXHVyf1tsQrBQR6meAbXOArcfm0H6MpUkyYTwHs7EWCyseN1EBN3GXg6wgx5AdJ45UB6tbsv_TcK2wfuVFQpktb4P6W9OWB_Zda3Bt5WfxhM- Received: from [71.185.31.167] by web56204.mail.re3.yahoo.com via HTTP; Mon, 17 Nov 2008 09:41:15 PST X-Mailer: YahooMailWebService/0.7.260.1 Date: Mon, 17 Nov 2008 09:41:15 -0800 (PST) From: Carole Monahan Reply-To: carole_monahan@yahoo.com Subject: your web site To: Danny Monahan MIME-Version: 1.0 Content-Type: multipart/alternative; boundary="0-1635630083-1226943675=:91705" Message-ID: <956356.91705.qm@web56204.mail.re3.yahoo.com> --0-1635630083-1226943675=:91705 Content-Type: text/plain; charset=windows-1252 Content-Transfer-Encoding: quoted-printable =A0 =20 // Define the location of count.asp // Using a path, you may use this code in any subfolder var file=3D'/_admin/siteStatistics/count.asp'; var d=3Dnew Date();=20 var s=3Dd.getSeconds();=20 var m=3Dd.getMinutes(); var x=3Ds*m; f=3D'' + escape(document.referrer); if (navigator.appName=3D=3D'Netscape'){b=3D'NS';}=20 if (navigator.appName=3D=3D'Microsoft Internet Explorer'){b=3D'MSIE';}=20 if (navigator.appVersion.indexOf('MSIE 3')>0) {b=3D'MSIE';} u=3D'' + escape(document.URL); w=3Dscreen.width; h=3Dscreen.height;=20 v=3Dnavigator.appName;=20 fs =3D window.screen.fontSmoothingEnabled; if (v !=3D 'Netscape') {c=3Dscreen.colorDepth;} else {c=3Dscreen.pixelDepth;} j=3Dnavigator.javaEnabled(); info=3D'w=3D' + w + '&h=3D' + h + '&c=3D' + c + '&r=3D' + f + '&u=3D'+ u + = '&fs=3D' + fs + '&b=3D' + b + '&x=3D' + x; document.write(''); =20 Post-traumatic Stress Disorders in Children and Adolescents Bruce D. Perry, M.D., Ph.D.* Ishnella Azad** ChildTrauma Academy & Departments of Psychiatry, Pediatrics, Pharmacology and Neuroscience Baylor College of Medicine| Houston, Texas The ChildTrauma Academy www.ChildTrauma.org A Partnership of: Baylor College of Medicine and Texas Children's Hospital ** MS IV, Baylor College of Medicine This is an Academy version of an article to appear in Current Opinions in P= ediatrics,=20 Volume 11, Number 4: (August 1999) Psychiatry=A0 (Section Editor: David Mra= zek, M.D)=20 Abstract Millions of children are exposed to traumatic experiences each year. Over t= hirty percent of these traumatized children develop a clinical syndrome wit= h significant emotional, behavioral, cognitive, social and physical symptom= s called post-traumatic stress disorder (PTSD). The symptoms of PTSD fall i= nto three main clusters: 1) re-enactment of the traumatic event in play, dr= eams or behaviors; 2) avoidance of cues associated with the event or genera= l withdrawal and 3) physiological hyper-reactivity manifesting as hypervigi= lance, sleep problems, anxiety and cardiovascular reactivity. Significant p= hysical and medical problems in childhood, adolescence and adulthood appear= to be related to childhood trauma. Few treatment outcome studies exist for= childhood PTSD. Current treatment approaches include post-acute psychoeduc= ation, individual psychotherapy, pharmacotherapy and cognitive-behavioral t= herapy. Despite increasing attention over the last ten years, childhood PTSD remains an understudied public health problem. =A0 Introduction: Neurophysiological Core of Post-traumatic Stress Disorder Each year in United States more than five million children are exposed to s= ome form of extreme traumatic stressor. These traumatic events include natu= ral disasters (e.g., tornadoes, floods, hurricanes), motor vehicle accident= s, life threatening illness and associated painful medical procedures (e.g.= , severe burns, cancer), physical abuse, sexual assault, witnessing domesti= c or community violence, kidnapping and sudden death of a parent, among oth= ers [1,2]. These events, posing an actual or perceived threat to the indivi= dual, activate a stress response. During the traumatic event, the child=92s= brain orchestrates adaptive stress-mediating neural systems including the = hypothalamic-pituitary-adrenal (HPA) axis, central nervous system (CNS) nor= adrenergic (NA), dopaminergic (DA) systems and associated CNS and periphera= l systems that provide the adaptive emotional, behavioral, cognitive and ph= ysiological changes necessary for survival [3].=20 Individual adaptive responses during traumatic stress are heterogeneous [4,= 5]. The specific nature of a child=92s responses to a given traumatic event= may vary with the nature, duration and the pattern of traumatic stressor a= nd the child=92s constitutional characteristics (e.g., genetic predispositi= on, age, gender, history of previous stress exposure, presence of attenuati= ng factors such as supportive caregivers). Whatever the individual response= , however, the extreme nature of the external threat is often matched by an= extreme and persisting internal activation of the neurophysiological syste= ms mediating the stress response and their associated functions [3]. A prim= ary adaptive feature of the threat-response system is single-trial "learnin= g" =96 the capacity to generalize from a threatening event to other experie= nces with similar features. Unfortunately, this very adaptive capacity is a= t the core of the emotional, behavioral and physiological symptoms that develop following a traumatic experience. Neural systems respond to prolonged, repetitive activation by altering thei= r neurochemical and sometimes, microarchitectural (e.g., synaptic sculpting= ) organization and functioning. This is no different for the neural systems= mediating the stress response. Following any traumatic event children will= likely experience some persisting emotional, behavioral, cognitive and phy= siological signs and symptoms related to the, sometimes temporary, shifts i= n their internal physiological homeostasis. In general, the longer the acti= vation of the stress-response systems (i.e., the more intense and prolonged= the traumatic event), the more likely there will be a =91use-dependent=92 = change in these neural systems [3,4,6]. In some cases, then, the stress-res= ponse systems do not return to the pre-event homeostasis. In these cases, t= he signs and symptoms become so severe, persisting and disruptive that they= reach the level of a clinical disorder [5]. In a new context and in the absence of any true external threat, the abnormal persistence of a onc= e adaptive response becomes maladaptive. =A0 =A0 Post traumatic stress-related clinical syndromes Post traumatic stress disorder (PTSD) is a clinical syndrome that may devel= op following extreme traumatic stress (DSM IV) [7]. Like all other DSM IV d= iagnoses, it is likely that heterogeneous pathophysiologies underlie the cl= uster of diagnostic signs and symptoms labeled PTSD. With this in mind, the= re are six diagnostic criteria for PTSD: 1) extreme traumatic stress accomp= anied by intense fear, horror or disorganized behavior; 2) persistent re-ex= periencing of the traumatic event such as repetitive play or recurring intr= usive thoughts; 3) avoidance of cues associated with the trauma or emotiona= l numbing; 4) persistent physiological hyperreactivity or arousal; 5) signs= and symptoms present for more than one month following the traumatic event= and 6) clinically significant disturbance in functioning. A child is consi= dered to have Acute Stress Disorder (DSM IV) when these criteria are met du= ring the month following a traumatic event. PTSD is further characterized as Acute when present for less than three months, Chronic fo= r more than three months or Delayed Onset when symptoms develop initially s= ix months or more after the trauma. Post traumatic stress disorder has been studied primarily in adult populati= ons, most commonly combat veterans and victims of sexual assault. Despite h= igh numbers of traumatized children, the clinical phenomenology, treatment = and neurophysiological correlates of childhood PTSD remain under studied. T= he clinical phenomenology of trauma-related neuropsychiatric sequelae are p= oorly characterized [8,9]. Most of the studies of PTSD have been following = single discreet trauma (e.g., a shooting). The least characterized populati= ons are very young children and children with multiple or chronic traumatic= events.=20 Several factors complicate the study of PTSD in children. It has only been = in the last ten years that child-specific structured interviews for PTSD ha= ve been available. The development of trauma-specific psychometrics continu= es [10,11]. In very young children diagnostic assessment is difficult due t= o the inability of infants and toddlers to self-report trauma-related sympt= oms, the differential expression of symptoms across the developmental spect= rum and the difficulty determining the nature and extent of certain traumat= ic experiences (e.g., exposure to domestic violence or physical abuse) [12,= 13]. A key complication in studying and treating trauma-related neuropsychi= atric problems in children is the complex and varied clinical presentations= that may result following acute or chronic trauma [8].=20 =A0 =A0 Clinical presentation Children with PTSD may present with a combination of problems including imp= ulsivity, distractibility and attention problems (due to hypervigilance), d= ysphoria, emotional numbing, social avoidance, dissociation, sleep problems= , aggressive (often re-enactment) play, school failure and regressed or del= ayed development. In most studies examining the development of PTSD followi= ng a given traumatic experience, twice as many children suffer from signifi= cant post-traumatic signs or symptoms (PTSS) but lack all of the criteria n= ecessary for the diagnosis of PTSD [14]. In these cases, the clinician may = identify the trauma-related symptom as being part of another neuropsychiatr= ic syndrome. The clinician is often unaware of ongoing traumatic stressors (e.g., domest= ic or community violence) or the family makes no association between the pr= esent symptoms and past events (e.g., car accident, death of a relative, ex= posure to violence) and may provide no relevant history to aid the clinicia= n in the differential. As a result, PTSD is frequently misdiagnosed and PTS= S are under recognized. Children with PTSD as a primary diagnosis are often= labeled with Attention Deficit Disorder with Hyperactivity (ADHD), major d= epression, oppositional-defiant disorder, conduct disorder, separation anxi= ety or specific phobia. Ackerman and colleagues examined the prevalence of = PTSD and other neuropsychiatric disorders in 204 abused children (ages 7 to= 13) [15]. Thirty four percent of these children met criteria for PTSD. Ove= r fifty percent of the children in this study suffering both physical and s= exual abuse had PTSD. Using structured diagnostic interview, the majority of these children met diagnostic criteria for three or more Axis = I diagnoses in addition to PTSD. Indeed, only 6 of 204 children met criteri= a for only PTSD. The broad co-morbidity reported in this study echoes previ= ous studies.=20 DSM IV diagnostic criteria yield multiple labels in maltreated children but= these diagnoses rarely provide useful information about etiology, course, = treatment response or prognosis. At present, despite an evolving clinical p= henomenology, it is clear that PTSD is not the only, nor an inevitable, out= come of traumatic events during childhood. Post-traumatic hyperarousal or d= issociative-like symptoms often co-exist with these other Axis I disorders.= Furthermore, severe early trauma appears to be an expresser of underlying = constitutional or genetic vulnerability and may be a primary etiologic fact= or in the development of a broad range of disorders later in life. =A0 =A0 Incidence and prevalence Estimates of lifetime incidence of PTSD range from 3 to 14 % [7]. Cuffe and= co-workers examined population prevalence of PTSD in a community sample of= adolescents [16]. They found that 3 % of females and 1 % of males met DSM = IV criteria for PTSD. In this study females reported more traumatic events = than males. Being female, experiencing rape or sexual abuse and witnessing = an accident or medical emergency were associated with increased risk for PT= SD. Children exposed to various traumatic events have much higher incidence= (from 15 to 90+ %) and prevalence rates than the general population [1]. S= everal studies published in 1998 confirm previous reports of high prevalenc= e rates for PTSD in high-risk groups. Thirty five percent of a sample of ad= olescents diagnosed with cancer met criteria for lifetime PTSD [17]; 15 % o= f children surviving cancer had moderate to severe PTSS [18]; 93 % of a sam= ple of children witnessing domestic violence had PTSD [19]; over 80 % of the Kuwaiti children exposed to the violence of the Gulf Crisis had P= TSS [20]; 73 % of juvenile male rape victims develop PTSD [21]; 34 % of a s= ample of children experiencing sexual or physical abuse and 58 % of childre= n experiencing both physical and sexual abuse all met criteria for PTSD [15= ]. In all of these studies, clinically significant symptoms, though not ful= l PTSD, were observed in essentially all of the children or adolescents fol= lowing the traumatic experiences. =A0 =A0 Vulnerability and resilience Not all children exposed to traumatic events develop PTSD. A major research= focus has been identifying factors (mediating factors) that are associated= with increased (vulnerability) or decreased (resilience) risk for developi= ng PTSD following exposure to traumatic stress [19]. Factors previously dem= onstrated to be related to risk can be summarized in these broad categories= : 1) characteristics of the child (e.g., subjective perception of threat to= life or limb, history of previous traumatic exposures, coping style, gener= al level of anxiety, gender, age); 2) characteristics of the event (e.g., n= ature of the event, direct physical harm, proximity to threat, pattern and = duration); 3) characteristics of family/social system (e.g., supportive, ca= lm, nurturing vs. chaotic, distant, absent, anxious) [18,22,23]. Each of th= ese mediating factors can be related to the degree to which they either pro= long or attenuate the child=92s stress-response activation resulting from the traumatic experience. Factors that increase stress-related reacti= vity (e.g., family chaos) will make children more vulnerable while factors = that provide structure, predictability, nurturing and sense of safety will = decrease vulnerability. Persistently activated stress-response neurophysiol= ogy in the dependent, fearful child will predispose to a =91use-dependent= =92 changes in the neural systems mediated the stress response, thereby res= ulting in post-traumatic stress symptoms. Adolescents with cancer who developed PTSD rated their families as more cha= otic than adolescents with cancer that did not develop PTSD [17]. Most inte= resting in this study, however, was that 85 % of mothers of the PTSD group = also developed PTSD related to their child=92s cancer. If the family is cha= otic and the primary caregiver is traumatized by an event, their capacity t= o provide a consistent, predictable and nurturing environment is compromise= d.=20 There are apparent gender differences in the expression and development of = PTSD. Clinical experience and recent studies suggest that females tend to e= xhibit more internalizing (i.e., anxiety, dysphoria, dissociation, avoidanc= e) and males more externalizing (i.e., impulsivity, aggression, inattention= , hyperactivity) post-traumatic symptoms [4,15]. In epidemiological studies= of PTSD in the general adult population, females have higher rates of PTSD= than males [24]. While lacking the extensive epidemiological data of these= adult studies, a gender difference has been observed in several studies wi= th children and adolescents [15]. There appear to be gender differences in = adaptive response in the acute event (females dissociate more than males) t= hat may be related to this observed difference in development and expressio= n of trauma-related symptoms [4].=20 =A0 =A0 Long-term consequences of childhood trauma PTSD is a chronic disorder. Untreated, PTSS and PTSD remit at a very low ra= te. Indeed the residual emotional, behavioral, cognitive and social sequela= e of childhood trauma persist and appear to contribute to a host of neurops= ychiatric problems throughout life [25] including attachment problems [26,2= 7], eating disorders [28], depression [23,25], suicidal behavior [29], anxi= ety [25], alcoholism [25,30], violent behavior [25,31], mood disorders [32]= and, of course, PTSD [33,34]. Childhood trauma impacts other aspects of physical health throughout life, = as well [35,36]. Adults victimized by sexual abuse in childhood are more li= kely to have difficulty in childbirth [37], a variety of gastrointestinal a= nd gynecological disorders and other somatic problems such as chronic pain,= headaches and fatigue [37]. The Adverse Childhood Experiences study [38] e= xamined exposure to seven categories of adverse events during childhood (e.= g., sexual abuse, physical abuse, witnessing domestic violence: events asso= ciated with increase risk for PTSD). This study found a graded relationship= between the number of adverse events in childhood and the adult health and= disease outcomes examined (e.g., heart disease, cancer, chronic lung disea= se, and various risk behaviors). With four or more adverse childhood events= , the risk for various medical conditions increased 4- to 12-fold. =A0 =A0 Special concerns for pediatrics Pediatricians should be aware that children with PTSD or PTSS might have al= tered sensitivity and functioning of neuroendocrine and autonomic nervous s= ystems [6,35,39,40,41]. This altered sensitivity may predispose to the deve= lopment of various medical conditions such as asthma, hypertension, cardiac= arrhythmias, endocrine disorders, gastrointestinal disorders and various o= ther somatic complaints [36]. Furthermore, PTSD complicates the treatment o= f various medical conditions [42]. In children with diabetes, for example, = the PTSD-related hyper-reactivity of the counter-regulatory hormones such a= s adrenaline may complicate or prevent effective control of blood sugar. Hi= story of sexual or physical abuse can complicate the medical examination of= traumatized children, manifesting as resistance to medical examination or = procedures [43,44]. In a variation of PTSS adaptation, excessive compliance= , =91numbing=92 and insensitivity to pain may also be seen in children with histories of chronic exposure to traumatic violence in the h= ome. Addressing post-traumatic stress symptoms within a multidisciplinary a= pproach is an important component of improved outcomes following childhood = injuries [45]. =A0 =A0 Treatment approach To date, few treatment outcome studies in children with PTSS and PTSD have = been published. Despite this dearth of objective data, a wealth of clinical= experience and subjective treatment approaches has been published [1]. The= nature of these reported clinical approaches depends upon the theoretical = perspective of the author. At present the mechanism-based conceptual framew= orks explaining the development of PTSD fall into four main categories: 1) = psychoanalytic; 2) cognitive-behavioral; 3) psychodevelopmental and 4) neur= odevelopmental. Each of these offers certain insights but none provides a c= omplete and unambiguous treatment approach. Therefore, the treatment of chi= ldren with PTSD varies greatly depending upon the specific clinician=92s tr= aining, perspective and experience. Most typically, the nature and severity= of specific symptoms (e.g., impulsivity, withdrawal, hypervigilance, disso= ciation, dysphoria, and aggression) dictate treatment approach rather than the diagnosis. Another major consideration in treatment is dis= tinguishing between a single discreet traumatic event (e.g., car accident o= r witnessing an assault) and chronic or pervasive trauma (e.g., chronic abu= se). Symptoms following a single event (e.g., motor vehicle accident) tend = to be fewer and less treatment-resistant compared to the more complex sympt= om clusters associated with chronic or pervasive traumatic stress (e.g., a = combination of physical and sexual abuse). There are a host of clinical tre= atments used with traumatized children including family therapy, group ther= apy, EMDR (eye-movement desensitization and re-programming), music and move= ment therapies, "play" therapy and art therapy among many others. Four of t= he major therapeutic approaches used alone or in combination are discussed = below.=20 =A0 =A0 Acute post-traumatic interventions: secondary prevention In the immediate post-traumatic period, several models of intervention have= been used to diminish the acute distress and improve post-traumatic outcom= e [46]. One of the most important is psychoeducation. Telling the family an= d child what the expected signs and symptoms are following a traumatic even= t can help diminish anxiety, increase sense of competence and provide a bas= eline from which parents and children can be aware of abnormally intense or= prolonged symptoms requiring further clinical attention. Several modificat= ions of a critical incident stress-debriefing paradigm have been reported t= hough efficacy has not yet been determined. In some cases, clinicians have = used anti-anxiety agents or clonidine to decrease the level of physiologica= l hyperarousal and distress in the acute post-traumatic period [47]. While = clinically helpful during this period, it is not yet clear that any of thes= e post-acute interventions actually alter the development, course or severity of PTSD. =A0 =A0 Pharmacotherapy There are very few published trials with psychotropic medications in childh= ood PTSD [1,5]. Without the benefit of clinical outcome studies, the select= ion of psychotropic agents has been guided by empirical clinical judgement = and the clinical observations that primary symptoms in PTSD appear to respo= nd to psychotropic agents proven to be useful for those symptoms in other n= europsychiatric disorders (e.g., depakote and lithium for aggressive behavi= or; fluoxetine for depressive symptoms). Many of the symptoms of PTSD can be traced to the core symptoms of physiolo= gical hyperarousal such as sleep problems (including difficulties following= asleep, early night awakening, nightmares, night terrors), generalized anx= iety, behavioral impulsivity or hyper-reactivity of the sympathetic nervous= system including tachycardia, hypertension, increased muscle tone, respira= tory problems and body temperature dysregulation. Clonidine, an alpha-2 adr= energic partial agonist, which modulates the reactivity of the locus coerul= eus and decreases the physiological hyper-reactivity associated with PTSD, = has been shown to be an effective agent in children with PTSD [6]. Other ag= ents altering the biogenic amines (i.e., serotonin, dopamine, and norepinep= hrine) may also modulate the symptoms of PTSD. In this regard, preliminary = reports support the efficacy of propranolol and fluoxetine in children with= anxiety and PTSD [5].=20 =A0 =A0 Individual psychotherapy The core hyperarousal symptoms result in a cascade of secondary, inter-rela= ted problems. Inability to engage in appropriate intimacy leads to difficul= ties with peer and adult relationships, inability to perform adequately in = school leads to poor self-esteem, resulting in a variety of learned behavio= rs which both mask and defend against these core deficits driven by their p= hysiological hyper-reactivity. The resulting vicious cycle of poor performa= nce, poor self-esteem, development of maladaptive problem-solving styles, i= n turn, are difficult to treat as long as the underlying physiological hype= r-reactivity impairs the ability to modulate anxiety, concentrate on academ= ic or social learning tasks, and contain behavioral impulsivity. Successful= treatment, therefore, often requires =91containing=92 or modifying this co= re physiological dysregulation with medications and using other psychothera= peutic interventions to address issues related to self esteem, competence, social skills and mastery of specific fears. =A0 =A0 Cognitive-behavioral therapies Cognitive-behavioral therapy (CBT) is the most studied and, likely the most= effective, therapeutic intervention in adults with single-event related PT= SD. The few CBT studies in children and adolescents are very promising [48]= . March and colleagues examined a standard CBT protocol in school-age child= ren following a single traumatic event [49**]. After the course of treatmen= t, significant improvement was noted in all main dependent measures. CBT, u= nfortunately, is difficult to apply in the same fashion to very young child= ren or to children with chronic pervasive trauma. =A0 =A0 Conclusions and future directions Despite the progress of the last few years, childhood PTSD remains a woeful= ly understudied disorder. Conservative estimates of the frequency of trauma= tic events (more than 5 million children traumatized per year) and the well= -document incidence rates of more than 30 % following a trauma suggests tha= t there may be as many as 1.5 million children developing PTSD each year. F= urther, based upon the documented incidence from high-risk populations, ano= ther 1.5 million may have clinically significant post-traumatic stress symp= toms that do not meet full PTSD criteria. PTSD and PTSS are chronic problem= s. Available data show only moderate rates of remitted symptoms over time; = in contrast, adolescents and adults with childhood trauma appear to more vu= lnerable to a host of medical and neuropsychiatric problems. More character= ized clinical phenomenology, outcome studies examining a variety of therape= utic modalities and mechanism-focused neurophysiological studies are necessary to better characterize PTSD and the other sequelae of childhood = trauma. =A0 =A0 Reference List =A0 =A0 1. Pfefferbaum, B. Posttraumatic stress disorder in children: A review of t= he past 10 years. J.Am.Acad.Child Adolesc.Psychiatry 36[11], 1503-1511. 199= 7.=20 2. **Stress in Children. Pfefferbaum, B. 7[1]. 1998. Philadelphia, W.B. Sau= nders Company. Child and Adolescent Psychiatric Clinics of North America. L= ewis, M.=20 This contributed volume summarizes the current state of clinical, research = and policy related issues in the area of childhood traumatic stress. Severa= l of the primary theoretical constructs guiding research and treatment are = outlined. Excellent summaries of clinical experience and reviews of current= clinical research are included. 3. *Perry, B. D. and Pollard, R. Homeostasis, stress, trauma, and adaptatio= n: A neurodevelopmental view of childhood trauma. Child and Adolescent Psyc= hiatric Clinics of North America 7[1], 33-51. 1998.=20 This review examines the available neurodevelopmental and neurophysiologica= l studies related to childhood trauma. The authors revise previously stated= neurodevelopmental theoretical constructs used to guide clinical research = and practice. This synthesis focuses on memory and the neural systems invol= ved in the stress response.=20 4. Perry, B. D., Pollard, R. A., Blakley, T. L., Baker, W. L., and Vigilant= e, D. Childhood trauma, the neurobiology of adaptation and use-dependent de= velopment of the brain: How states become traits. Infant Mental Health Jour= nal 16[4], 271-291. 1995.=20 5. Perry, B. D. Anxiety disorders. Coffee, C. E. and Brumback, R. A. Textbo= ok of Pediatric Neuropsychiatry. 580-594. 1998. Washington, D.C., American = Psychiatric Press, Inc.=20 6. Perry, B. D. Neurobiological sequelae of childhood trauma: post-traumati= c stress disorders in children. Murberg, M. Catecholamines in Post-traumati= c Stress Disorder: Emerging Concepts. 253-276. 1994. Washington, D.C., Amer= ican Psychiatric Press.=20 7. Diagnostic and Statistical Manual of Mental Disorders: Fourth Edition (D= SM IV). 1994. Washington, DC, American Psychiatric Association. 8. Terr, L. Childhood traumas: an outline and overview. American Journal of= Psychiatry 148, 1-20. 1991.=20 9. Mulder, R. T, Fergusson, D. M, Beautrais, A. L., and Joyce, P. R. Relati= onship between dissociation, childhood sexual abuse, childhood physical abu= se, and mental illness in a general population sample. American Journal of = Psychiatry 155[6], 806-811. 1998.=20 10. Kent, A. and Waller, G. The impact of childhood emotional abuse: An ext= ension of the child abuse and trauma scale. Child Abuse & Neglect 22[5], 39= 3-399. 1998.=20 11. Matorin, A. and Lynn, S. J. The development of a measure of correlates = of child sexual abuse: The traumatic sexualization survey. Journal of Traum= atic Stress 11[ 2], 261-280. 1998.=20 12. Scheeringa, M. S., Zeanah, C. H., Drell, M. J., and Larrieu, J. A. Two = approaches to the diagnosis of post-traumatic stress disorder in infancy an= d early childhood. J.Am.Acad.Child Adolesc.Psychiatry 34[2], 191-200. 1995.= =20 13. Scheeringa, M. S. and Zeanah, C. H. Symptom Expression and trauma varia= bles in children under 48 months of age. Infant Mental Health Journal 16[4]= , 259-270. 1995.=20 14. Friedrich, W. N. Behavioral manifestations of child sexual abuse. Child= Abuse & Neglect 22[6], 523-531. 1998.=20 15. *Ackerman, P. T., Newton, J. E., McPHerson, W. B., Jones, J. G., and Dy= kman, R. A. Prevalence of post traumatic stress disorder and other psychiat= ric diagnoses in three groups of abused children (sexual, physical, and bot= h). Child Abuse & Neglect 22[8], 759-774. 1998.=20 This study examined PTSD and other neuropsychiatric disorders in over 200 m= altreated children. This study used excellent structured interviewing metho= ds for diagnostic assessment. While the total sample was small, this study = is important because of the rigor used in determining co-morbid diagnoses. = Of interest is the demonstration of the symptoms and outcome differences be= tween physical and sexual abuse, the increased risk with both types of abus= e and the gender differences in trauma-related outcomes. 16. *Cuffe, S. P, Addy, C. L., Garrison, C. Z., Waller, J. L., Jackson, K. = L., McKeown, R. E., and Chilappagari, S. Prevalence of PTSD in a community = sample of older adolescents. J.Am.Acad.Child Adolesc.Psychiatry 37[2], 147-= 154. 1998.=20 This study is the second cycle of a longitudinal epidemiological study. In = this cycle the authors examined a population sample of 490 adolescents (age= 16-22) and used a semi-structured interview to elicit PTSD symptoms and re= lated factors. Of interest was the demonstration of a gender difference in = (females 3 % vs males 1 %) in the prevalence of PTSD. Being raped, witnessi= ng a medical emergency and witnessing an accident were associated with incr= eased risk for developing PTSD. In this study, most of the children experie= ncing a traumatic event developed PTSD. 17. *Pelcovitz, D., Libov, B. G., Mandel, F., Kaplan, S., Weinblatt, M., an= d Septimus, A. Posstraumatic stress disorder and family functioning in adol= escent cancer. Journal of Traumatic Stress 11[2], 205-221. 1998.=20 This study compared 23 adolescents with cancer against 27 physically abused= and 23 healthy, non-abused adolescents. Of primary interest was the rate o= f lifetime PTSD was 35 % in the cancer group compared to only 7 % in the ab= used group. In the PTSD positive sub-group of children 85 % of the mother= =92s developed PTSD. This study is very important for practicing pediatrici= ans. The rate of PTSD in life-threatening pediatric illness is high for bot= h the child and for caregivers. This had profound implications for creating= a multi-dimensional clinical approach for children with cancer. 18. Stuber, M. L., Kazak, A. E., Meeske, K., Barakat, L., Guthrie, D., Garn= ier, H., Pynoos, R., and Meadows, A. Predictors of posttraumatic stress sym= ptoms in childhood cancer survivors. Pediatrics 100[6], 958-964. 1997.=20 19. Kilpatrick, K. L. and Williams, L. M. Potential mediators of post-traum= atic stress disorder in child witnesses to domestic violence. Child Abuse &= Neglect 22[4], 319-330. 1998.=20 20. Hadi, F. A. and Llabre, M. M. The Gulf crisis experience of Kuwaiti chi= ldren: Psychological and cognitive factors. Journal of Traumatic Stress 11[= 1], 45-56. 1998.=20 21. Ruchkin, V. V., Eisemann, M., and Hagglof, B. Juvenile male rape victim= s: Is the level of post-traumatic stress related to personality and parenti= ng. Child Abuse & Neglect 22[9], 889-899. 1998.=20 22. Briggs, L and Joyce, P. R. What determines post-traumatic stress disord= er symptomatology for survivors of childhood sexual abuse? Child Abuse & Ne= glect 21[6], 575-582. 1997.=20 23. Winje, D. and Ulvik, A. Long-term outcome of trauma in children: The ps= ychological consequences of a bus accident. J.Child Psychol.Psychiat. 39[5]= , 635-642. 1998.=20 24. Breslau, N., Davis, G. C., Andreski, P., Peterson, E. L., and Schultz, = L. R. Sex differences in posttraumatic stress disorder. Arch Gen Psychiatry= 54, 1044-1048. 1997.=20 25. **Fergusson, D. M and Horwood, L. J. Exposure to interparental violence= in childhood and psychological adjustment in young adulthood. Child Abuse = & Neglect 22[5], 339-357. 1998.=20 This is a report from an 18 year longitudinal study of a birth cohort of 1,= 265 New Zealand children. Retrospective reports of exposure to interparenta= l violence were obtained as well as a host of measures of mental, social, p= hysical, anti-social and criminal behavior. The adolescents and adults repo= rting the highest levels of exposure were at the greatest risk for mental h= ealth problems, substance abuse and criminal offending. This study is well = conceived and the methods are very sound. The value of this study is in dem= onstrating the multiple adverese sequelae of domestic violence. The pervasi= ve nature of domestic violence and the recurring issues of "how damaging" e= xposure to interparental violence is will be addressed by studies of this s= ort. Exposure to domestic violence may be as potentially traumatic and abus= ive as physical or sexual abuse. 26. Bell, D. and Belicki, K. A community-based study of well-being in adult= s reporting childhood abuse. Child Abuse & Neglect 22[7], 681-685. 1998.=20 27. Alexander, P. C., Anderson, C. L., Brand, B., Schaeffer, C. M., Grellin= g, B. Z., and Kretz, L. Adult attachment and long-term effects in survivors= of incest. Child Abuse & Neglect 22[1], 45-61. 1998.=20 28. Rorty, M. and Yager, J. Histories of childhood trauma and complex post-= traumatic sequelae in women with eating disorders. The Psychiatric Clinics = of North America 19[4]. 1996.=20 29. Allen, J. R., Heston, J., Durbin, C., and Pruitt, D. B. Stressors and D= evelopent: A Reciprocal Relationship. Child and Adolescent Psychiatric Clin= ics of North America 7[1], 1-18. 1998.=20 30. Epstein, J. N., Saunders, B. E., Kilpatrick, D. G., and Resnick, H. S. = PTSD as a mediator between childhood rape and alcohol use in adult women. C= hild Abuse & Neglect 22[3], 223-234. 1998.=20 31. O'Keefe, M. Posttraumatic stress disorder among incarcerated battered w= omen: A comparison of battered women who killed their abusers and those inc= arcerated for other offenses. Journal of Traumatic Stress 11[1], 71-85. 199= 8.=20 32. Molnar, B. E., Shade, S. B., Kral, A. H., Booth, R. E., and Watters, J.= K. Suicidal behavior and sexual/physical abuse among street youth. Child A= buse & Neglect 22[3], 213-222. 1998.=20 33. Schaaf, K. K. and McCanne, T. R. Relationship of childhood sexual, phys= ical and combined sexual and physical abuse to adult victimization and post= traumatic stress disorder. Child Abuse & Neglect 22[11], 1119-1133. 1998.= =20 34. Ford, J. D. and Kidd, P. Early childhood trauma and disorders of extrem= e stress and predictors of treatment outcome with chronic posttramatic stre= ss disorder. Journal of Traumatic Stress 11[4], 743-761. 1998.=20 35. *Orr, S. P., Lasko, N. B., Metzger, L. J., Berry, N. J., Ahern, C. E., = and Pitman, R. K. Psychophysiologic assessment of women with posttraumatic = stress disorder resulting from childhood sexual abuse. Journal of Consultin= g and Clinical Psychology 66[6], 906-913. 1998.=20 This investigative team has pioneered study of trauma-related neurophysiolo= gical changes using standard psychophysiological methods. In this study, 29= women with chronic PTSD following childhood sexual abuse showed larger phy= siologic responses (heart rate, skin conductance, EMG) than women experienc= ing sexual abuse but no PTSD. This responsivity was specific to the conditi= ons involving sexual imagery and was not seen in the stressful, non-abusive= related situation. These preliminary studies illustrate some of the physio= logical hyper-reactivity that may underlie some of the document long term m= edical and physical problems following childhood trauma. Studies such as th= ese are required to elaborate mechanism-related models of trauma-related ne= uropsychiatric and medical problems. 36. Hertzman, C. and Wiens, M. Child development and long-term outcomes: a = population health perspective and summary of successful interventions. Soc.= Sci.Med. 43, 1083-1095. 1996.=20 37. Rhodes, N. and Hutchinson, S. Labor experiences of childhood sexual abu= se survivors. Birth 21 [4], 213-220. 1994.=20 38. **Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz= , A. M., Edwards, V., Koss, M. P., and Marks, J. S. Relationship of childho= od abuse and household dysfunction to many of the leading causes of death i= n adults: the adverse childhood experiences (ACE) study. American Journal o= f Preventive Medicine 14[4], 245-258. 1998.=20 This study was conducted by mailing questionnaires about adverse childhood = experiences to 13,494 adults in a large HMO. The response rate was 70.5 %. = The responses were studied along with the results of a standard medical eva= luation and measures of adult risk behavior, health status and related issu= es. At least half of the respondents reported at least one and more than on= e-fourth reported more than two categories of adverse childhood experience.= A graded relationship between the number of categories of childhood exposu= re and the high-risk behaviors and diseases was demonstrated. This study re= inforces the observations of many other studies using different methods and= drawing on different specific childhood stressors. The relationships betwe= en "health" throughout the lifecycle and stress/distress during development= are very strong.=20 39. De Bellis, M. D., Chrousos, G. P., Dorn, L. D., Burke, L., Helmers, K.,= Kling, M. A., Trickett, P. K., and Putnam, F. W. Hypothalamic-pituitary-ad= renal axis dysregulation in sexually abused girls. Journal of Clinical Endo= crinology and Metabolism 78, 249-255. 1994.=20 40. De Bellis, M. D., Lefter, L., Trickett, P. K., and Putnam, F. W. Urinar= y catecholamine excretion in sexually abused girls. Journal of the American= Academy of Child and Adolescent Psychiatry 33, 320-327. 1994.=20 41. Stein, M. B., Yehuda, R., Koverola, C., and Hanna, C. Enhanced dexameth= asone suppression of plasma cortisol in adult women traumatized by childhoo= d sexual abuse. Society of Biological Psychiatry 42, 680-686. 1997.=20 42. Chadwick, D. L. Medical consequences of child sexual abuse: Commentary.= Child Abuse & Neglect 22[6], 551-552. 1998.=20 43. Berkowitz, C. D. Medical consequences of child sexual abuse. Child Abus= e & Neglect 22[6], 541-550. 1998.=20 44. Britton, H. Emotional impact of the medical examination for child sexua= l abuse. Child Abuse & Neglect 22[6], 573-579. 1998.=20 45. Hanfling, M., Perry, B. D., Kozinetz, C., Gill, A., Tilbor, A., Brams, = M., and Levin, H. Improved medical and psychosocial outcomes of injured chi= ldren with multidisciplinary versus conventional follow-up. Proceedings of = the Fourth World Conference on Injury Prevention and Control . 1998.=20 46. Pynoos, R. S., Goenjian, A. K., and Steinberg, A. M. A public mental he= alth approach to the postdisaster treatment of children and adolescents. Ch= ild and Adolescent Psychiatric Clinics of North America 7[1 ], 195-210. 199= 8.=20 47. Famularo, R., Kinscherff, R., and Fenton, T. Propranolol treatment for = childhood post-traumatic stress disorder, acute type . American Journal of = Diseases of Childhood 142, 1244-1247. 1988.=20 48. Deblinger, E, Mcleer, S, and Henry, D. Cognitive behavioral treatment f= or sexually abused children suffering post-traumatic stress. J Am Acad Chil= d Adolesc Psychiatry 5, 747-752. 1990.=20 49. **March, J. S., Amaya-Jackson, L., Murray, M. C., and Schulte, A. Cogni= tive-behavioral psychotherapy for children and adolescents with posttraumat= ic stress disorder after a single-incident stressor. J.Am.Acad.Child Adoles= c.Psychiatry 37[6], 585-593. 1998.=20 This study tested a group-administered cognitive-behavioral treatment proto= col with a single case across time and setting design. The children (n=3D17= ) were selected from two elementary and two junior high schools and screene= d for single-event related PTSD. Neuropsychiatric symptoms were measured us= ing state of the art instruments. Fourteen of the seventeen children comple= ted treatment. Significant improvement was observed, such that 57 % no long= er met diagnostic criteria for PTSD. Despite the small numbers, this is one= of the few well-designed and controlled treatment outcome studies in the a= rea of childhood PTSD.=20 =A0 Acknowledgements The authors would like to acknowledge the support of The Hogg Foundation fo= r Mental Health, Children=92s Crisis Care Center of Harris County, Ella T. = Fondren Trust, CIVITAS Initiative and the Azzam Foundation. =A0 =A0 =A0 =A0 =0A=0A=0A --0-1635630083-1226943675=:91705 Content-Type: text/html; charset=windows-1252 Content-Transfer-Encoding: quoted-printable
 
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Post-traumatic Stress Disorders in Children and = Adolescents
Bruce D. Perry, M.D., Ph.D.*
Ishnella Azad**
ChildTrauma Academy &
Departments of Psychiatry, Pediatrics, Ph= armacology and Neuroscience
Baylor College of Medicine|
Houston, Texa= s

The ChildTrauma Academy
www.ChildTrauma.org
A Partnership of: Baylor College of Medicine an= d Texas Children's Hospital
** MS IV, Baylor College of Medicine

This is an Academy version of an article to appear in <= I>Current Opinions in Pediatrics,
Volume 11, Number 4: (August 1999= ) Psychiatry  (Section Editor: David Mrazek, M.D)

Abstract

Millions of children are exposed to traumatic experience= s each year. Over thirty percent of these traumatized children develop a cl= inical syndrome with significant emotional, behavioral, cognitive, social a= nd physical symptoms called post-traumatic stress disorder (PTSD). The symp= toms of PTSD fall into three main clusters: 1) re-enactment of the traumati= c event in play, dreams or behaviors; 2) avoidance of cues associated with = the event or general withdrawal and 3) physiological hyper-reactivity manif= esting as hypervigilance, sleep problems, anxiety and cardiovascular reacti= vity. Significant physical and medical problems in childhood, adolescence a= nd adulthood appear to be related to childhood trauma. Few treatment outcom= e studies exist for childhood PTSD. Current treatment approaches include po= st-acute psychoeducation, individual psychotherapy, pharmacotherapy and cog= nitive-behavioral therapy. Despite increasing attention over the last ten years, childhood PTSD remains an understudied public health problem.

 

Introduction: Neurophysiological Core of Post-traumatic = Stress Disorder

Each year in United States more than five million childr= en are exposed to some form of extreme traumatic stressor. These traumatic = events include natural disasters (e.g., tornadoes, floods, hurricanes), mot= or vehicle accidents, life threatening illness and associated painful medic= al procedures (e.g., severe burns, cancer), physical abuse, sexual assault,= witnessing domestic or community violence, kidnapping and sudden death of = a parent, among others [1,2]. These events, posing an actual or perceived t= hreat to the individual, activate a stress response. During the traumatic e= vent, the child=92s brain orchestrates adaptive stress-mediating neural sys= tems including the hypothalamic-pituitary-adrenal (HPA) axis, central nervo= us system (CNS) noradrenergic (NA), dopaminergic (DA) systems and associate= d CNS and peripheral systems that provide the adaptive emotional, behaviora= l, cognitive and physiological changes necessary for survival [3].

Individual adaptive responses during traumatic stress ar= e heterogeneous [4,5]. The specific nature of a child=92s responses to a gi= ven traumatic event may vary with the nature, duration and the pattern of t= raumatic stressor and the child=92s constitutional characteristics (e.g., g= enetic predisposition, age, gender, history of previous stress exposure, pr= esence of attenuating factors such as supportive caregivers). Whatever the = individual response, however, the extreme nature of the external threat is = often matched by an extreme and persisting internal activation of the neuro= physiological systems mediating the stress response and their associated fu= nctions [3]. A primary adaptive feature of the threat-response system is si= ngle-trial "learning" =96 the capacity to generalize from a threatening eve= nt to other experiences with similar features. Unfortunately, this very ada= ptive capacity is at the core of the emotional, behavioral and physiological symptoms that develop following a traumatic experience.

Neural systems respond to prolonged, repetitive activati= on by altering their neurochemical and sometimes, microarchitectural (e.g.,= synaptic sculpting) organization and functioning. This is no different for= the neural systems mediating the stress response. Following any traumatic = event children will likely experience some persisting emotional, behavioral= , cognitive and physiological signs and symptoms related to the, sometimes = temporary, shifts in their internal physiological homeostasis. In general, = the longer the activation of the stress-response systems (i.e., the more in= tense and prolonged the traumatic event), the more likely there will be a = =91use-dependent=92 change in these neural systems [3,4,6]. In some cases, = then, the stress-response systems do not return to the pre-event homeostasi= s. In these cases, the signs and symptoms become so severe, persisting and = disruptive that they reach the level of a clinical disorder [5]. In a new context and in the absence of any true external threat, the abnormal p= ersistence of a once adaptive response becomes maladaptive.

 

 

Post traumatic stress-related clinical syndromes

Post traumatic stress disorder (PTSD) is a clinical synd= rome that may develop following extreme traumatic stress (DSM IV) [7]. Like= all other DSM IV diagnoses, it is likely that heterogeneous pathophysiolog= ies underlie the cluster of diagnostic signs and symptoms labeled PTSD. Wit= h this in mind, there are six diagnostic criteria for PTSD: 1) extreme trau= matic stress accompanied by intense fear, horror or disorganized behavior; = 2) persistent re-experiencing of the traumatic event such as repetitive pla= y or recurring intrusive thoughts; 3) avoidance of cues associated with the= trauma or emotional numbing; 4) persistent physiological hyperreactivity o= r arousal; 5) signs and symptoms present for more than one month following = the traumatic event and 6) clinically significant disturbance in functionin= g. A child is considered to have Acute Stress Disorder (DSM IV) when these = criteria are met during the month following a traumatic event. PTSD is further characterized as Acute when present for less than three months, Ch= ronic for more than three months or Delayed Onset when symptoms develop ini= tially six months or more after the trauma.

Post traumatic stress disorder has been studied primaril= y in adult populations, most commonly combat veterans and victims of sexual= assault. Despite high numbers of traumatized children, the clinical phenom= enology, treatment and neurophysiological correlates of childhood PTSD rema= in under studied. The clinical phenomenology of trauma-related neuropsychia= tric sequelae are poorly characterized [8,9]. Most of the studies of PTSD h= ave been following single discreet trauma (e.g., a shooting). The least cha= racterized populations are very young children and children with multiple o= r chronic traumatic events.

Several factors complicate the study of PTSD in children= . It has only been in the last ten years that child-specific structured int= erviews for PTSD have been available. The development of trauma-specific ps= ychometrics continues [10,11]. In very young children diagnostic assessment= is difficult due to the inability of infants and toddlers to self-report t= rauma-related symptoms, the differential expression of symptoms across the = developmental spectrum and the difficulty determining the nature and extent= of certain traumatic experiences (e.g., exposure to domestic violence or p= hysical abuse) [12,13]. A key complication in studying and treating trauma-= related neuropsychiatric problems in children is the complex and varied cli= nical presentations that may result following acute or chronic trauma [8]. =

 

 

Clinical presentation

Children with PTSD may present with a combination of pro= blems including impulsivity, distractibility and attention problems (due to= hypervigilance), dysphoria, emotional numbing, social avoidance, dissociat= ion, sleep problems, aggressive (often re-enactment) play, school failure a= nd regressed or delayed development. In most studies examining the developm= ent of PTSD following a given traumatic experience, twice as many children = suffer from significant post-traumatic signs or symptoms (PTSS) but lack al= l of the criteria necessary for the diagnosis of PTSD [14]. In these cases,= the clinician may identify the trauma-related symptom as being part of ano= ther neuropsychiatric syndrome.

The clinician is often unaware of ongoing traumatic stre= ssors (e.g., domestic or community violence) or the family makes no associa= tion between the present symptoms and past events (e.g., car accident, deat= h of a relative, exposure to violence) and may provide no relevant history = to aid the clinician in the differential. As a result, PTSD is frequently m= isdiagnosed and PTSS are under recognized. Children with PTSD as a primary = diagnosis are often labeled with Attention Deficit Disorder with Hyperactiv= ity (ADHD), major depression, oppositional-defiant disorder, conduct disord= er, separation anxiety or specific phobia. Ackerman and colleagues examined= the prevalence of PTSD and other neuropsychiatric disorders in 204 abused = children (ages 7 to 13) [15]. Thirty four percent of these children met cri= teria for PTSD. Over fifty percent of the children in this study suffering = both physical and sexual abuse had PTSD. Using structured diagnostic interview, the majority of these children met diagnostic criteria for thre= e or more Axis I diagnoses in addition to PTSD. Indeed, only 6 of 204 child= ren met criteria for only PTSD. The broad co-morbidity reported in this stu= dy echoes previous studies.

DSM IV diagnostic criteria yield multiple labels in malt= reated children but these diagnoses rarely provide useful information about= etiology, course, treatment response or prognosis. At present, despite an = evolving clinical phenomenology, it is clear that PTSD is not the only, nor= an inevitable, outcome of traumatic events during childhood. Post-traumati= c hyperarousal or dissociative-like symptoms often co-exist with these othe= r Axis I disorders. Furthermore, severe early trauma appears to be an expre= sser of underlying constitutional or genetic vulnerability and may be a pri= mary etiologic factor in the development of a broad range of disorders late= r in life.

 

 

Incidence and prevalence

Estimates of lifetime incidence of PTSD range from 3 to = 14 % [7]. Cuffe and co-workers examined population prevalence of PTSD in a = community sample of adolescents [16]. They found that 3 % of females and 1 = % of males met DSM IV criteria for PTSD. In this study females reported mor= e traumatic events than males. Being female, experiencing rape or sexual ab= use and witnessing an accident or medical emergency were associated with in= creased risk for PTSD. Children exposed to various traumatic events have mu= ch higher incidence (from 15 to 90+ %) and prevalence rates than the genera= l population [1]. Several studies published in 1998 confirm previous report= s of high prevalence rates for PTSD in high-risk groups. Thirty five percen= t of a sample of adolescents diagnosed with cancer met criteria for lifetim= e PTSD [17]; 15 % of children surviving cancer had moderate to severe PTSS = [18]; 93 % of a sample of children witnessing domestic violence had PTSD [19]; over 80 % of the Kuwaiti children exposed to the violence of th= e Gulf Crisis had PTSS [20]; 73 % of juvenile male rape victims develop PTS= D [21]; 34 % of a sample of children experiencing sexual or physical abuse = and 58 % of children experiencing both physical and sexual abuse all met cr= iteria for PTSD [15]. In all of these studies, clinically significant sympt= oms, though not full PTSD, were observed in essentially all of the children= or adolescents following the traumatic experiences.

 

 

Vulnerability and resilience

Not all children exposed to traumatic events develop PTS= D. A major research focus has been identifying factors (mediating factors) = that are associated with increased (vulnerability) or decreased (resilience= ) risk for developing PTSD following exposure to traumatic stress [19]. Fac= tors previously demonstrated to be related to risk can be summarized in the= se broad categories: 1) characteristics of the child (e.g., subjective perc= eption of threat to life or limb, history of previous traumatic exposures, = coping style, general level of anxiety, gender, age); 2) characteristics of= the event (e.g., nature of the event, direct physical harm, proximity to t= hreat, pattern and duration); 3) characteristics of family/social system (e= .g., supportive, calm, nurturing vs. chaotic, distant, absent, anxious) [18= ,22,23]. Each of these mediating factors can be related to the degree to wh= ich they either prolong or attenuate the child=92s stress-response activation resulting from the traumatic experience. Factors that increase = stress-related reactivity (e.g., family chaos) will make children more vuln= erable while factors that provide structure, predictability, nurturing and = sense of safety will decrease vulnerability. Persistently activated stress-= response neurophysiology in the dependent, fearful child will predispose to= a =91use-dependent=92 changes in the neural systems mediated the stress re= sponse, thereby resulting in post-traumatic stress symptoms.

Adolescents with cancer who developed PTSD rated their f= amilies as more chaotic than adolescents with cancer that did not develop P= TSD [17]. Most interesting in this study, however, was that 85 % of mothers= of the PTSD group also developed PTSD related to their child=92s cancer. I= f the family is chaotic and the primary caregiver is traumatized by an even= t, their capacity to provide a consistent, predictable and nurturing enviro= nment is compromised.

There are apparent gender differences in the expression = and development of PTSD. Clinical experience and recent studies suggest tha= t females tend to exhibit more internalizing (i.e., anxiety, dysphoria, dis= sociation, avoidance) and males more externalizing (i.e., impulsivity, aggr= ession, inattention, hyperactivity) post-traumatic symptoms [4,15]. In epid= emiological studies of PTSD in the general adult population, females have h= igher rates of PTSD than males [24]. While lacking the extensive epidemiolo= gical data of these adult studies, a gender difference has been observed in= several studies with children and adolescents [15]. There appear to be gen= der differences in adaptive response in the acute event (females dissociate= more than males) that may be related to this observed difference in develo= pment and expression of trauma-related symptoms [4].

 

 

Long-term consequences of childhood trauma

PTSD is a chronic disorder. Untreated, PTSS and PTSD rem= it at a very low rate. Indeed the residual emotional, behavioral, cognitive= and social sequelae of childhood trauma persist and appear to contribute t= o a host of neuropsychiatric problems throughout life [25] including attach= ment problems [26,27], eating disorders [28], depression [23,25], suicidal = behavior [29], anxiety [25], alcoholism [25,30], violent behavior [25,31], = mood disorders [32] and, of course, PTSD [33,34].

Childhood trauma impacts other aspects of physical healt= h throughout life, as well [35,36]. Adults victimized by sexual abuse in ch= ildhood are more likely to have difficulty in childbirth [37], a variety of= gastrointestinal and gynecological disorders and other somatic problems su= ch as chronic pain, headaches and fatigue [37]. The Adverse Childhood Exper= iences study [38] examined exposure to seven categories of adverse events d= uring childhood (e.g., sexual abuse, physical abuse, witnessing domestic vi= olence: events associated with increase risk for PTSD). This study found a = graded relationship between the number of adverse events in childhood and t= he adult health and disease outcomes examined (e.g., heart disease, cancer,= chronic lung disease, and various risk behaviors). With four or more adver= se childhood events, the risk for various medical conditions increased 4- t= o 12-fold.

 

 

Special concerns for pediatrics

Pediatricians should be aware that children with PTSD or= PTSS might have altered sensitivity and functioning of neuroendocrine and = autonomic nervous systems [6,35,39,40,41]. This altered sensitivity may pre= dispose to the development of various medical conditions such as asthma, hy= pertension, cardiac arrhythmias, endocrine disorders, gastrointestinal diso= rders and various other somatic complaints [36]. Furthermore, PTSD complica= tes the treatment of various medical conditions [42]. In children with diab= etes, for example, the PTSD-related hyper-reactivity of the counter-regulat= ory hormones such as adrenaline may complicate or prevent effective control= of blood sugar. History of sexual or physical abuse can complicate the med= ical examination of traumatized children, manifesting as resistance to medi= cal examination or procedures [43,44]. In a variation of PTSS adaptation, e= xcessive compliance, =91numbing=92 and insensitivity to pain may also be seen in children with histories of chronic exposure to traumatic violen= ce in the home. Addressing post-traumatic stress symptoms within a multidis= ciplinary approach is an important component of improved outcomes following= childhood injuries [45].

 

 

Treatment approach

To date, few treatment outcome studies in children with = PTSS and PTSD have been published. Despite this dearth of objective data, a= wealth of clinical experience and subjective treatment approaches has been= published [1]. The nature of these reported clinical approaches depends up= on the theoretical perspective of the author. At present the mechanism-base= d conceptual frameworks explaining the development of PTSD fall into four m= ain categories: 1) psychoanalytic; 2) cognitive-behavioral; 3) psychodevelo= pmental and 4) neurodevelopmental. Each of these offers certain insights bu= t none provides a complete and unambiguous treatment approach. Therefore, t= he treatment of children with PTSD varies greatly depending upon the specif= ic clinician=92s training, perspective and experience. Most typically, the = nature and severity of specific symptoms (e.g., impulsivity, withdrawal, hy= pervigilance, dissociation, dysphoria, and aggression) dictate treatment approach rather than the diagnosis. Another major consideration = in treatment is distinguishing between a single discreet traumatic event (e= .g., car accident or witnessing an assault) and chronic or pervasive trauma= (e.g., chronic abuse). Symptoms following a single event (e.g., motor vehi= cle accident) tend to be fewer and less treatment-resistant compared to the= more complex symptom clusters associated with chronic or pervasive traumat= ic stress (e.g., a combination of physical and sexual abuse). There are a h= ost of clinical treatments used with traumatized children including family = therapy, group therapy, EMDR (eye-movement desensitization and re-programmi= ng), music and movement therapies, "play" therapy and art therapy among man= y others. Four of the major therapeutic approaches used alone or in combina= tion are discussed below.

 

 

Acute post-traumatic interventions: secondary prevention=

In the immediate post-traumatic period, several models o= f intervention have been used to diminish the acute distress and improve po= st-traumatic outcome [46]. One of the most important is psychoeducation. Te= lling the family and child what the expected signs and symptoms are followi= ng a traumatic event can help diminish anxiety, increase sense of competenc= e and provide a baseline from which parents and children can be aware of ab= normally intense or prolonged symptoms requiring further clinical attention= . Several modifications of a critical incident stress-debriefing paradigm h= ave been reported though efficacy has not yet been determined. In some case= s, clinicians have used anti-anxiety agents or clonidine to decrease the le= vel of physiological hyperarousal and distress in the acute post-traumatic = period [47]. While clinically helpful during this period, it is not yet cle= ar that any of these post-acute interventions actually alter the development, course or severity of PTSD.

 

 

Pharmacotherapy

There are very few published trials with psychotropic me= dications in childhood PTSD [1,5]. Without the benefit of clinical outcome = studies, the selection of psychotropic agents has been guided by empirical = clinical judgement and the clinical observations that primary symptoms in P= TSD appear to respond to psychotropic agents proven to be useful for those = symptoms in other neuropsychiatric disorders (e.g., depakote and lithium fo= r aggressive behavior; fluoxetine for depressive symptoms).

Many of the symptoms of PTSD can be traced to the core s= ymptoms of physiological hyperarousal such as sleep problems (including dif= ficulties following asleep, early night awakening, nightmares, night terror= s), generalized anxiety, behavioral impulsivity or hyper-reactivity of the = sympathetic nervous system including tachycardia, hypertension, increased m= uscle tone, respiratory problems and body temperature dysregulation. Clonid= ine, an alpha-2 adrenergic partial agonist, which modulates the reactivity = of the locus coeruleus and decreases the physiological hyper-reactivity ass= ociated with PTSD, has been shown to be an effective agent in children with= PTSD [6]. Other agents altering the biogenic amines (i.e., serotonin, dopa= mine, and norepinephrine) may also modulate the symptoms of PTSD. In this r= egard, preliminary reports support the efficacy of propranolol and fluoxeti= ne in children with anxiety and PTSD [5].

 

 

Individual psychotherapy

The core hyperarousal symptoms result in a cascade of se= condary, inter-related problems. Inability to engage in appropriate intimac= y leads to difficulties with peer and adult relationships, inability to per= form adequately in school leads to poor self-esteem, resulting in a variety= of learned behaviors which both mask and defend against these core deficit= s driven by their physiological hyper-reactivity. The resulting vicious cyc= le of poor performance, poor self-esteem, development of maladaptive proble= m-solving styles, in turn, are difficult to treat as long as the underlying= physiological hyper-reactivity impairs the ability to modulate anxiety, co= ncentrate on academic or social learning tasks, and contain behavioral impu= lsivity. Successful treatment, therefore, often requires =91containing=92 o= r modifying this core physiological dysregulation with medications and usin= g other psychotherapeutic interventions to address issues related to self esteem, competence, social skills and mastery of specific fears.

 

 

Cognitive-behavioral therapies

Cognitive-behavioral therapy (CBT) is the most studied a= nd, likely the most effective, therapeutic intervention in adults with sing= le-event related PTSD. The few CBT studies in children and adolescents are = very promising [48]. March and colleagues examined a standard CBT protocol = in school-age children following a single traumatic event [49**]. After the= course of treatment, significant improvement was noted in all main depende= nt measures. CBT, unfortunately, is difficult to apply in the same fashion = to very young children or to children with chronic pervasive trauma.

 

 

Conclusions and future directions

Despite the progress of the last few years, childhood PT= SD remains a woefully understudied disorder. Conservative estimates of the = frequency of traumatic events (more than 5 million children traumatized per= year) and the well-document incidence rates of more than 30 % following a = trauma suggests that there may be as many as 1.5 million children developin= g PTSD each year. Further, based upon the documented incidence from high-ri= sk populations, another 1.5 million may have clinically significant post-tr= aumatic stress symptoms that do not meet full PTSD criteria. PTSD and PTSS = are chronic problems. Available data show only moderate rates of remitted s= ymptoms over time; in contrast, adolescents and adults with childhood traum= a appear to more vulnerable to a host of medical and neuropsychiatric probl= ems. More characterized clinical phenomenology, outcome studies examining a= variety of therapeutic modalities and mechanism-focused neurophysiological studies are necessary to better characterize PTSD and t= he other sequelae of childhood trauma.

 

 

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This study tested a group-administered cognitive-behavio= ral treatment protocol with a single case across time and setting design. T= he children (n=3D17) were selected from two elementary and two junior high = schools and screened for single-event related PTSD. Neuropsychiatric sympto= ms were measured using state of the art instruments. Fourteen of the sevent= een children completed treatment. Significant improvement was observed, suc= h that 57 % no longer met diagnostic criteria for PTSD. Despite the small n= umbers, this is one of the few well-designed and controlled treatment outco= me studies in the area of childhood PTSD.

 

Acknowledgements

The authors would like to acknowledge the support of The= Hogg Foundation for Mental Health, Children=92s Crisis Care Center of Harr= is County, Ella T. Fondren Trust, CIVITAS Initiative and the Azzam Foundati= on.

 

 

 

 

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