Updated: Mar 4, 2008
Posttraumatic stress disorder (PTSD) in children and adolescents occurs as a result of a child's exposure to one or more traumatic events that were life-threatening or perceived to be likely to cause serious injury to self or others. In addition, the child or adolescent must have responded with intense fear, helplessness, or horror. Traumatic events can take many forms, including physical or sexual assaults, natural disasters, traumatic death of a loved one, or emotional abuse or neglect. Severe emotional trauma has widespread effects on children's development, in that it clearly obliterates the belief that their parents will protect them. The premature destruction of these beliefs can have profound negative consequences on development.
Traumatized children and adolescents are understandably frequently preoccupied with danger and vulnerability, sometimes leading to misperceptions of danger, even in situations that are not threatening. Multiple researchers (eg, Kardiner, van der Kolk1 ) note that, once posttraumatic stress symptoms emerge, PTSD leads to neurophysiologic correlates that impact brain function in developing children and adolescents.
In 1980, the term PTSD first came into existence in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III).2 Only in 1987 did the DSM series make reference to traumatized children. The first major studies of the effects of large traumas on children were Bloch's 1956 study of the effect of a tornado in Mississippi, Lacey's 1972 study of the effects of an avalanche on a Welsh school, Newman's 1976 work on the Buffalo Creek disaster,3 and Terr's 1979 research on the Chowchilla bus kidnapping.4
Evidence indicates a genetic predisposition for PTSD, suggesting that it may be linked to the individual's temperament and to reactivity of the hypothalamic pituitary axis.
Lifetime prevalence of PTSD is 8%.5 The incidence and course of PTSD vary and depend on various factors, including the type of trauma, the proximity to the stressor, and the reaction of the child's parents. After being kidnapped, witnessing the death of a parent, or suffering domestic violence, the rate of PTSD may be 95-100%. Following a sniper attack at school, 40% of children experienced moderate-to-severe PTSD. In one study of children in foster care, 64% who had experienced sexual abuse had PTSD, and 42% who had experienced physical abuse fulfilled the PTSD criteria. Moreover, 18% of the children who were not abused also met PTSD criteria, presumably because they had witnessed violence.
The prevalence in a location overwhelmingly depends on the endemicity of violence in the region.
Alone, PTSD is not a fatal disorder. Nevertheless, it frequently leads to conduct disorder, substance abuse, depression, and risk-taking that poses considerable danger.
PTSD has a considerable morbidity rate, particularly for children. In addition to the symptoms of numbing, hyperarousal, and recollections of the event that adults experience, children suffer from a decreased ability to participate in the normal academic and social activities of childhood. Therefore, a traumatic event can send a child down a new developmental path, one that is less favorable than the one the child was previously on.
A host of emotional and behavioral problems frequently arise as a result of PTSD and are not part of the criteria for categorical diagnosis. These include disruptive behavior disorders, eating disorders, sexual acting out, other risk-taking activities, depression, the full range of anxiety disorders, dissociation, mood lability, violence, and difficulty concentrating.
Studies of adults who were sexually or physically abused as children demonstrate significantly higher rates of PTSD (72-100%) than studies of children who were abused (21-55%). This finding indicates that the full impact of abuse may not be experienced until a child reaches adulthood, engages in adult relationships and responsibilities, and develops more sophisticated cognitive capabilities.
No major racial predominance is observed; however, PTSD is more common among individuals in low socioeconomic groups and among those living in areas in which violence is endemic.
PTSD is more common in women than in men.
PTSD occurs in people of all ages, but younger and elderly persons are the most vulnerable.
Diagnostic criteria
Diagnosing posttraumatic stress disorder in children
| Acanthocytosis | Oppositional Defiant Disorder |
| Attention Deficit Hyperactivity Disorder | Personality Disorder: Borderline |
| Conduct Disorder | |
| Mood Disorder: Bipolar Disorder | |
| Mood Disorder: Depression |
Many problems are comorbid with posttraumatic stress disorder (PTSD) and need to be considered when PTSD is found. These comorbid disorders include depression, childhood disruptive disorders, the full range of anxiety disorders, substance abuse, and sexual acting out. Furthermore, in the presence of these other disorders, the possibility of PTSD should be considered.
Numerous psychological tests may be helpful in assessing posttraumatic stress disorder (PTSD); some are directly designed to evaluate for PTSD symptoms, and others are designed to examine symptoms of related disorders. The following tests may be helpful:
Selective serotonin reuptake inhibitors (SSRIs) are the medications of choice in managing anxiety, depression, avoidance behavior, and intrusive recollections. Beta-blockers and alpha-adrenergic agonists (eg, guanfacine, clonidine) are helpful in reducing arousal, decreasing forced reexperiencing of the trauma, and avoiding the neurophysiologic kindling that can contribute to chronic illness. These medications are most helpful if used very soon after the onset of symptoms.
Mood stabilizers can be helpful in dealing with increased arousal, impulsivity, and already established kindling once the illness has become chronic. The mood stabilizers are not interchangeable. Carbamazepine may ameliorate persistent reexperiencing of the event, whereas valproic acid may ameliorate symptoms of avoidance.
Atypical antipsychotics are infrequently used compared with the medications listed above. They should only be used for patients unresponsive to other medications or when marked agitation or psychosis is present.
These agents are the first-line medications for managing anxiety, depression, avoidance behavior, and intrusive recollections. Antidepressant agents chemically unrelated to the tricyclic, tetracyclic, or other available antidepressants. They inhibit CNS neuronal uptake of serotonin (5HT) and may also have a weak effect on norepinephrine and dopamine neuronal reuptake.
SSRIs are greatly preferred to the other classes of antidepressants because the adverse effect profile of SSRIs is less prominent and improved compliance is promoted. SSRIs do not have the cardiac arrhythmia risk associated with tricyclic antidepressants. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered when treating a child or adolescent with mood disorder.
Physicians are advised to be aware of the following information and to use appropriate caution when considering treatment with SSRIs in the pediatric population.
In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory that most SSRIs are not suitable for use by persons younger than 18 years for treatment of "depressive illness." After review, this agency decided that the risks to pediatric patients outweigh the benefits of treatment with SSRIs, except fluoxetine (Prozac), which appears to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.
In October 2003, the US Food and Drug Administration (FDA) issued a public health advisory regarding reports of suicidality in pediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. The FDA has asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and thus could not be definitively linked to drug treatment.
However, a study of more than 65,000 children and adults treated for depression between 1992 and 2002 by the Group Health Cooperative in Seattle found that suicide risk declines, not rises, with the use of antidepressants.7 This is the largest study to date to address this issue.
Currently, evidence does not associate obsessive compulsive disorder (OCD) and other anxiety disorders treated with SSRIs with an increased risk of suicide.
FDA approved for OCD in children >6 y. FDA approved for PTSD in adults. PO liquid concentrate available.
50 mg/d PO; may increase after 1 wk; usual effective dose is 50-200 mg/d; not to exceed 200 mg/d
<6 years: Not established
6-12 years: 25 mg/d PO, not to exceed 200 mg/d
>12 years: 12.5 mg PO qd, may increase gradually qwk; not to exceed adult dose
Inhibits CYP2C9, CYP2C19, CYP3A4, and, to a lesser extent, CYP2D6 and CYP1A2
Increases toxicity of MAOIs, diazepam, tolbutamide, tryptophan, and warfarin; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); discontinue other serotonergic agents at least 2 wk before beginning SSRIs
Documented hypersensitivity; do not use within 14 d of MAOIs
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in preexisting seizure disorders, recent MI, unstable heart disease, and hepatic and renal impairment
Common adverse effects in children include insomnia, agitation, somnolence, upset stomach, and headache; sexual dysfunction may occur; causes more GI upset and diarrhea than other SSRIs; may cause rash, which requires discontinuing medication; may cause restlessness, anorexia, weight change, and nightmares; libido dampening and sexual dysfunction in adolescents can occur
FDA approved for depression and OCD in children and adolescents. Half-life is 7-9 d. Most activating of SSRIs. Some believe most effective for depression. Many people require adjuvant medication to help sleep (eg, trazodone 100 mg). Liquid formulation available.
10-20 mg/d PO initially, with a dose of 20 mg after 1 wk; may increase up to 80 mg/d prn; typical dose is 20 mg/d
<8 years: Not established
>8 years: 10 mg/d PO initially, may increase to 20 mg/d PO after 1 wk; although higher doses have been used for children with OCD, they have not been shown beneficial in PTSD
Potent inhibitor of CYP3A4; also inhibits CYP2C9, CYP2C19, and CYP2D6 to a lesser degree
Increases toxicity of diazepam and trazodone by decreasing clearance; also increases toxicity of MAOIs, thioridazine, and highly protein-bound drugs; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan); discontinue other serotonergic agents at least 2 wk before beginning SSRIs
Documented hypersensitivity; do not use within 14 d of stopping MAOIs or initiate MAOIs within 6 wk of stopping fluoxetine; do not initiate thioridazine within 6 wk of fluoxetine
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment and history of seizures; common adverse effects include insomnia, headaches, upset stomach, nausea, vomiting, tremor, and sexual dysfunction; social disinhibition, agitation, and mania may occur
Not approved by FDA for use in children. PO susp available.
10 mg/d PO initially; increase to 20 mg/d after 1 wk; not to exceed 80 mg/d
Limited data suggest 5-10 mg/d PO initially; may increase gradually prn; not to exceed 20 mg/d
Inhibits CYP450 2D6, thus may increase toxicity of 2D6 substrates (eg, phenothiazines, propafenone, flecainide and encainide, other SSRIs, tricyclic antidepressants); phenobarbital and phenytoin decrease effects of paroxetine; alcohol, cimetidine, sertraline, phenothiazines, and warfarin increase toxicity of paroxetine; serotonin syndrome (ie, myoclonus, rigidity, confusion, nausea, hyperthermia, autonomic instability, coma, eventual death) occurs with simultaneous use of other serotonergic agents (eg, anorectic agents, tramadol, buspirone, trazodone, clomipramine, nefazodone, tryptophan), discontinue other serotonergic agents at least 2 wk prior to using other SSRIs
Documented hypersensitivity; concurrent administration with MAOIs or administering within 14 d of discontinuing MAOIs; coadministration with thioridazine or pimozide
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Newborn infants exposed to SSRIs during the third trimester of pregnancy have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding; preliminary analysis of a retrospective study shows increased congential malformations as a whole, particularly for cardiovascular malformations, with paroxetine compared to other antidepressants with exposure during the first trimester
Caution in history of seizures, mania, renal disease, and cardiac disease; commonly causes weight gain and sexual dysfunction; bupropion can restore libido, and sildenafil can restore potency
Headache and abdominal discomfort are generally mild and transient (approximately 1 wk), although they can require cessation of therapy
Newest SSRI. Appears to have the most benign side effect profile, with fewer sexual adverse effects than other SSRIs. Not FDA approved for children. PO solution available.
10-20 mg/d PO initially; 30 mg usually is needed for full effect
Not established; limited data suggest 5-10 mg/d PO for younger children
Coadministration with cimetidine increases levels; do not use within 14 d of MAOIs; caution with coadministration of other serotonergic drugs
Documented hypersensitivity; MAOIs within 14 d
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in history of seizures, mania, renal disease, and cardiac disease is prudent given what is known of SSRIs; adverse effect profile shows it is the least likely SSRI to cause sexual adverse effects
These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.
May be useful for treatment of hyperarousal.
10-120 mg PO tid
Up to 2.5 mg/kg/d PO divided tid
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, or rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol
Increases levels of neuroleptics (eg, chlorpromazine, thioridazine); may increase effects of hydralazine, haloperidol, and benzodiazepines
Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities; asthma
C - Safety for use during pregnancy has not been established.
Caution in diabetes mellitus (may cause hypoglycemia or hyperglycemia and mask signs of hypoglycemia) and hyperthyroidism; beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; adverse effects include depression, decreased energy, and, possibly, decreased mental acuity
The centrally acting antihypertensives clonidine and guanfacine have been used to treat children with attention deficit hyperactivity disorder. An inhibition of norepinephrine release in the brain may be the mechanism of action.
Not approved by FDA for any psychiatric uses in children. Available in tab or transdermal skin patches. Frequently given to children. Affects alpha1-, alpha2-, and alpha3-adrenergic receptors.
0.05 mg/d PO initially; may increase by 0.05 mg q3-4d until dose reaches 0.1-0.3 mg/d PO divided tid
Limited data suggest 0.15-0.3 mg/d PO divided tid
Concurrent CNS depressants may increase effects; TCAs may decrease levels; sudden death reported in coadministration with methylphenidate hs
Documented hypersensitivity; cardiovascular disease; depressive symptoms
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment; check ECG before use and after dosage increases; common adverse effects include drowsiness, depression, dry mouth, dysphoria, and photophobia; less common adverse effects are headache, abdominal pain, nosebleeds, irritability, decreased glucose tolerance, and exacerbation of existing arrhythmias; discontinue slowly to avoid cardiac rhythm problems
Action similar to clonidine, but has a longer half-life and less sedation. More selective alpha-agonist. Not recommended for children <12 y. Effects alpha2-adrenergic receptors only.
0.5 mg/d PO initially; may increase by 0.5 mg q3d until desired effect reached; typical dose is 1-3 mg/d PO divided bid/tid
Not established
Increases effect of other hypotensive agents; TCAs may decrease hypotensive effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in hepatic impairment, severe coronary insufficiency, and recent MI; check ECG before use and after dosage increases; drowsiness may occur but less problematic than with clonidine; may cause depression, dysphoria, photophobia, and dry mouth; less common adverse effects are headache, abdominal pain, nosebleeds, irritability, decreased glucose tolerance, and exacerbation of existing arrhythmias; discontinue slowly to avoid cardiac rhythm problems
These agents are helpful in dealing with increased arousal, impulsivity, and already established kindling when posttraumatic stress disorder (PTSD) becomes chronic.
Initially used as an antiseizure medication and mood stabilizer. Also used for explosive outbursts.
200 mg/d PO divided doses initially; may increase by increments of 100 mg/d twice per wk; if adverse effects occur, decrease dose by 200 mg
Dose range is 300-1600 mg/d PO; monitor plasma levels (ie, 4-12 mcg/mL) to maintain dose within therapeutic range
6-12 years: 100 mg/d PO divided bid initially; may increase by 100 mg/d qwk
Maintenance: 20-30 mg/kg/d PO divided bid/qid; not to exceed 1000 mg/d
>12 years: Administer as in adults to achieve plasma level of 8-12 mcg/mL
Halothane coadministration may cause hepatocellular damage; grapefruit juice, influenza vaccine, isoniazid, cimetidine, erythromycin, and phenelzine increase plasma levels; phenytoin, alprazolam, clonazepam, primidone, and phenobarbital decrease CBZ level and levels of interacting agents; fluoxetine increases level
Decreases levels of imipramine, phenothiazines, haloperidol, theophylline, thyroid hormones, ritonavir, saquinavir, contraceptives, risperidone, thiothixene, cyclosporine, corticosteroids, doxycycline, trazodone, doxepin, and amitriptyline
Increases plasma levels of diltiazem and verapamil; can reduce its own level by autoinduction; coadministration with lithium or loxapine increases toxicity of CBZ and the interacting agents; coadministration with clozapine further increases bone marrow toxicity and resulting agranulocytosis
Documented hypersensitivity; MAOIs within 14 d; history of liver disease, cardiovascular disease, or blood dyscrasias
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Slight but significant risk of causing agranulocytosis or aplastic anemia during drug initiation; avoid using hazardous equipment or driving; other depressants and alcohol may lead to increased dizziness and sleepiness; keep in a dry place; drinking grapefruit juice while taking CBZ elevates blood levels; report any indications of blood dyscrasias (eg, easy bruising, sore throats, fever, rash)
May cause sedation, blood dyscrasias including aplastic anemia, exfoliative dermatitis, nausea, vomiting, dizziness, ataxia, diplopia, nystagmus, tics, muscle cramps, decreased thyroid function, hepatitis, renal impairment, urinary incontinence, hair loss, motor and vocal tics, rash, interstitial pneumonitis, cardiac conduction delay, SIADH, and lenticular opacities
Adverse behavioral reactions may occur during the first mo, including mania, extreme irritability, agitation, insomnia, obsessive thinking, hallucinations, delirium, psychosis, paranoia, hyperactivity and aggression, and memory problems
Useful in certain types of epilepsy, bipolar disorder, migraine headaches, impulsivity, dissociation, and PTSD. Extended-release (ie, qd administration) form is available. Requires higher dosing because 80% absorbed.
250 mg PO tid initially; may increase dose gradually until level of 50-125 mcg/mL achieved
Maintenance: 750-3000 mg/d PO in divided doses
Panic episode: 20 mg/kg PO q12h for 2 doses initially; then 10 mg/kg bid
Maintenance: 500-3500 mg/d PO to achieve plasma level of 50-125 mcg/mL
10-15 mg/kg/d PO divided bid/tid initially; increase by 5-10 mg/kg/d PO qwk until therapeutic plasma level achieved
Maintenance: 30-60 mg/kg/d PO divided bid/tid
Inhibits CYP2C19, 2C9, and 2D6Coadministration with cimetidine, salicylates, felbamate, erythromycin, and SSRIs may increase toxicity; rifampin may reduce valproate levels significantly; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates
Coadministration with carbamazepine may cause variable changes of carbamazepine concentrations, with possible loss of seizure control; may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels, while either one may decrease valproate levels; may displace warfarin from protein binding sites (monitor coagulation tests); may increase zidovudine levels
Documented hypersensitivity; hepatic disease or dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Monitor for hepatic toxicity (obtain liver function tests before initiating therapy and 3-6 mo thereafter); increase LFTs (3 times that of baseline is common and not a problem); most dangerous if used in very young children; serum ammonia levels may increase independently of other liver functions and may cause altered mental status; check platelet count and bleeding times before therapy and during treatment; may cause pancreatitis (monitor accordingly)
Advise patient to immediately report any abdominal pain; may cause erythema multiforme
Adverse effects include sedation, GI upset (treat with H2 blocker), weight gain, liver toxicity, blood dyscrasias, alopecia, tremor, ataxia, platelet problems, impaired cognitive function, and hyperammonemia
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PTSD, post traumatic stress disorder, posttraumatic stress syndrome, trauma, traumatic event, emotional trauma, disorders of extreme stress, conduct disorder, substance abuse, depression, eating disorders, behavioral disorders, sexual acting out, depression, anxiety disorders, posttraumatic play, nightmares, night terrors, dissociative phenomena, personality change, social withdrawal, impaired relationships, rape, sexual abuse, childhood disruptive disorders
Roy H Lubit, MD, PhD, Assistant Clinical Professor, Mount Sinai School of Medicine; Clinical Faculty, Department of Child Psychiatry, New York University School of Medicine; Private Practice
Disclosure: Nothing to disclose.
Angelo P Giardino, MD, PhD, Clinical Associate Professor, Department of Pediatrics, Baylor College of Medicine; Medical Director, Texas Children's Health Plan, Inc
Angelo P Giardino, MD, PhD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Professional Society on the Abuse of Children, Harris County Medical Society, Helfer Society, and International Society for Prevention of Child Abuse and Neglect
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Carrie Sylvester, MD, MPH, Director of Education in Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Pediatrics, Northwestern University Medical School
Carrie Sylvester, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Pediatrics, American Medical Women's Association, American Psychiatric Association, and American Society for Adolescent Psychiatry
Disclosure: Nothing to disclose.
Caroly Pataki, MD, Professor of Clinical Psychiatry and Behavioral Sciences, Department of Psychiatry, Division Chair, Child and Adolescent Psychiatry, Director of Training, Child and Adolescent Psychiatry Residency Program, University of Southern California Keck School of Medicine
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
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