Introduction
Background
The formal diagnosis of posttraumatic stress disorder (PTSD) was not introduced into the Diagnostic and Statistical Manual of Mental Disorders until its third publication in 1980. In earlier DSM editions, this relatively new diagnosis was characterized as stress response syndrome, a type of gross stress reaction, or a situational disorder, and often incorrectly associated with personal weakness instead of situational trauma.
PTSD is now defined as a pathological anxiety that usually occurs after an individual experiences or witnesses severe trauma that constitutes a threat to the physical integrity or life of the individual or of another person.
The individual initially responds with intense fear, helplessness, or horror. The person later develops a response to the event that is characterized by persistently reexperiencing the event, with resultant symptoms of numbness, avoidance, and hyperarousal. These symptoms result in clinically significant distress or functional impairment. To meet the full criteria for PTSD, these symptoms should be present for a minimum of 1 month following the initial traumatic event.
The events experienced may be natural disasters, violent personal assaults, war, severe automobile accidents, or the diagnosis of a life-threatening condition. For children, a developmentally inappropriate sexual experience may be considered a traumatic event, even though it may not have actually involved violence or physical injury.
PTSD can be acute (symptoms lasting <3 mo), chronic (symptoms lasting >3 mo), or of delayed onset (6 mo elapses from event to symptom onset).
Recent studies have pointed to a new dissociative subtype of PTSD that has clinical and neurobiological features that distinguish it from the nondissociative PTSD. This dissociative subtype is described as an overmodulation of affect, or a form of emotion dysregulation, and is mediated by midline prefrontal inhibition of limbic regions. These findings are important in the treatment of PTSD because patients can now be assessed for dissociative symptoms and treated accordingly.1
An image of the brain structures involved in dealing with fear and stress can be seen below.
Brain structures involved in dealing with fear and stress.
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Brain structures involved in dealing with fear and stress.
Pathophysiology
The amygdala is a key brain structure implicated in PTSD. Research has shown that exposure to traumatic stimuli can lead to fear conditioning with resultant activation of the amygdala and associated structures such as the hypothalamus, locus ceruleus, periaqueductal gray, and parabrachial nucleus. This activation and the accompanying autonomic neurotransmitter and endocrine activity produce many of the symptoms of PTSD. The orbitoprefrontal cortex exerts an inhibiting effect on this activation. The hippocampus also may have a modulating effect on the amygdala. However, in people who develop PTSD, the orbitoprefrontal cortex appears less capable of inhibiting this activation, possibly due to stress-induced atrophy of specific nuclei in this region.
Frequency
United States
PTSD has a lifetime prevalence of 8-10% and accounts for considerable disability and morbidity. One study found the prevalence of PTSD in a sample of adolescent boys to be 3.7% and adolescent girls to be 6.3%.2 Approximately 30% of men and women who have spent time in a war zone experience PTSD.3
Mortality/Morbidity
In various studies, a direct relationship is observed between the severity of the trauma and the risk for PTSD.4
Individuals with the disorder may have an increased risk of impulsive behavior, suicide, and homicide. Victims of sexual assault are at especially high risk for developing mental health problems and committing suicide.
One of the most pivotal observations in relation to the development of PTSD in adults who were traumatized as children is the association between early trauma exposure and subsequent retraumatization.5
Studies conducted with veteran participants from Operation Iraqi Freedom and Operation Enduring Freedom (Afghanistan) determined a strong correlation between duration of combat exposure and PTSD. Service members from Operation Enduring Freedom (Afghanistan) reported less combat experience and, consequently, a lower incidence of mental health disorder compared with veterans of Operation Iraqi Freedom, who reported greater combat exposure.6,7
Sex
Females may be at a higher risk than males. An epidemiologic survey of adult women indicates alarmingly high rates of traumatic events, particularly those events relating to being victims of crimes. Sexual assault probably has the most impact on women, and trauma from combat probably has the most impact on men.
Although earlier veteran studies have been somewhat inconsistent, recent studies suggest that Operation Iraqi Freedom service confers equal PTSD risk to both genders, with the duration and severity of combat experience having a greater influence upon the likelihood of developing PTSD.8,9
Age
PTSD can occur in persons of any age, including children. Symptoms usually begin within 3 months of the event, although a delay of months or years may occur before symptoms appear.
Clinical
History
One study found that nearly half (48%) of the patients in general medical practices with posttraumatic stress disorder (PTSD) were receiving no mental health treatment at the time of intake to the study. The most common reason patients gave for not receiving medication was the failure of physicians to recommend such treatment.10
The information elicited from the interview with the patient must satisfy certain diagnostic criteria to make the formal diagnosis. As with many diagnoses, PTSD can be subclinical, in which the criteria are almost but not fully met. Diagnosis is based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. The mental status examination should routinely consist of questions about exposure to trauma or abuse.
The first criterion has 2 components, as follows:
Experiencing, witnessing, or being confronted with an event involving serious injury, death, or a threat to a person's physical integrity
A response involving helplessness, intense fear, or horror (sometimes expressed in children as agitation or disorganized behavior)
The second major criterion involves the persistent reexperiencing of the event in one of several ways. This may involve thoughts or perception, images, dreams, illusions, hallucinations, dissociative flashback episodes, or intense psychological distress or reactivity to cues that symbolize some aspect of the event. However, children reexperience the event through repetitive play, not through perception like adults.
The third diagnostic criterion involves avoidance of stimuli that are associated with the trauma and numbing of general responsiveness; this is determined by the presence of 3 or more of the following:
Avoidance of thoughts, feelings, or conversations that are associated with the event
Avoidance of people, places, or activities that may trigger recollections of the event
Inability to recall important aspects of the event
Significantly diminished interest or participation in important activities
Feeling of detachment from others
Narrowed range of affect
Sense of having a foreshortened future
The fourth criterion is symptoms of hyperarousal, and 2 or more of the following symptoms are required to fulfill this criterion:
Difficulty sleeping or falling asleep
Decreased concentration
Hypervigilance
Outbursts of anger or irritable mood
Exaggerated startle response
Fifth, the duration of the relevant criteria symptoms should be more than 1 month, as opposed to acute stress disorder, for which the criterion is a duration of less than 1 month.
Finally, the disturbance is a cause of clinically significant distress or impairment in functioning.
Children may have different reactions to trauma than adults. For children aged 5 years or younger, typical reactions can include a fear of being separated from a parent, crying, whimpering, screaming, immobility and/or aimless motion, trembling, frightened facial expressions, and excessive clinging. Parents may also notice regressive behaviors. Children of this age tend to be strongly affected by their parents' reactions to the traumatic event.11
Children aged 6-11 years may show extreme withdrawal, disruptive behavior, and/or an inability to pay attention. Regressive behaviors, nightmares, sleep problems, irrational fears, irritability, refusal to attend school, outbursts of anger, and fighting are also common. The child may have somatic complaints with no medical basis. Schoolwork often suffers. Also, depression, anxiety, feelings of guilt, and emotional numbing are often present. Adolescents aged 12-17 years may have responses similar to adults.11
Physical
Patients may present with physical injuries from the traumatic event (eg, bruises in victims of domestic abuse). Patients with chronic PTSD may present with somatic complaints and, possibly, general medical conditions. Special attention should be paid to the patient's sleep hygiene. Recent studies suggest that even a single cognitive behavior treatment (CBT) for sleep abnormalities can significantly improve daytime PTSD symptoms, as can pharmacological treatments for sleep abnormalities.12,13
Mental Status Examination
General appearance may be affected. Patients may appear disheveled and have poor personal hygiene.
Behavior may be altered. Patients may appear agitated, and their startle reaction may be extreme.
Orientation is sometimes affected. The patient may report episodes of not knowing the current place or time, even though this may not have been evident during the interview.
Memory is likely to be affected. Patients may report forgetfulness, especially concerning the specific details of the traumatic event. A recent pilot study suggests memory abnormalities may not be limited to the traumatic event itself.14
Concentration is poor.
Impulse control is poor.
Speech rate and flow may be altered.
Mood and affect may be changed. Patients may have feelings of depression, anxiety, guilt, and/or fear.
Thoughts and perception may be affected. Patients may be more concerned with the content of hallucinations, delusions, suicidal ideation, phobias, and reliving the experience; certain patients may become homicidal. Potential for suicide and homicide must be noted as part of the mental status.
Causes
PTSD is caused by experiencing, witnessing, or being confronted with an event involving serious injury, death, or threat to the physical integrity of an individual, along with a response involving helplessness and/or intense fear or horror. The more severe the trauma and the more intense the acute stress symptoms, the higher the risk for PTSD. When these events involve an individual with a physiologic vulnerability based on genetic (inherited) contributions and other personal characteristics, PTSD results. These personal characteristics include prior exposure to trauma, childhood adversity (eg, separation from parents), and preexisting anxiety or depression.
Researchers have identified factors that interact to influence vulnerability to developing PTSD.15 16 These factors include the following:
Characteristics of the trauma exposure itself - Proximity to, severity of, and duration of exposure to the trauma
Characteristics of the individual - Prior trauma exposures, family history or prior psychiatric illness, and sex (Women are at greatest risk for many of the most common assertive traumas.)
Posttrauma factors - Availability of social support, emergence of avoidance or numbing, hyperarousal, and reexperiencing symptoms. For reexperiencing symptoms, specifically, a pilot monozygotal twin study shows that patients with PTSD have impaired extinction of novel conditioned fear stimuli.Differential Diagnoses
Anxiety Disorders
Obsessive-Compulsive Disorder
Schizophrenia
Other Problems to Be Considered
Acute stress disorder
Adjustment disorder
Malingering (must be excluded)
Mood disorder with psychotic features
Psychotic disorders caused by a general medical condition
Substance-induced disorders
Workup
Laboratory Studies
Cortisol levels may be decreased, norepinephrine and epinephrine levels may be elevated, and hypothalamic-pituitary-adrenal axis activity may be abnormal; however, these findings are still only used for research.
Natural opiates, which are produced by the body to mask pain in the face of danger, may be found in higher levels in people with PTSD, even after the danger has passed. This may lead to the blunted emotions seen in persons with this condition.
Imaging Studies
MRI studies of the brain suggest that the amount of hippocampal atrophy correlates with the intensity of PTSD symptoms, but MRI is still not a recommended diagnostic test.14 Some studies in monozygotic twins show that a small hippocampus may be a predisposing factor to the later development of PTSD in the face of a stressor.18
Other Tests
Although increased arousal is not a required criterion for diagnosis, it might be measurable through studies of autonomic functioning (eg, heart rate monitoring, electromyography, sweat gland activity).
In children, the combination of an elevated heart rate 24-hours post trauma and a novel survey, the Child Trauma Screening Questionnaire, identified children likely to develop PTSD with adequate sensitivity, and with high specificity and negative predictive values at 1- and 6-months post trauma.Treatment
Medical Care
Many of the complications and disability associated with prolonged posttraumatic stress disorder (PTSD) may be prevented by initiating the assessment and treatment quickly after the traumatic event, well before a diagnosis of PTSD can be made.
Treatment is often best accomplished with a combination of pharmacologic and nonpharmacologic therapies. Medications may be required to control the physiological symptoms, which can enable the patient to tolerate and work through the highly emotional material in psychotherapy.
Treatment is often complicated by comorbid disorders.
If present, alcohol or substance abuse problems should be the initial focus of treatment.
In the presence of coexisting depression, treatment should focus on the PTSD because its course, biology, and treatment response are unlike those associated with major depression.
Treatment consists of group therapy, individual and family therapy, cognitive behavioral therapy, play therapy, art therapy, anxiety management, eye movement desensitization and reprocessing (EMDR), and relaxation techniques. A recent meta-analysis of studies in adults with PTSD revealed trauma-focused CBT and EMDR should be first-line nonpharmacologic therapies for PTSD.20,21
For adolescents and children, treatment is primarily psychotherapeutic in nature.
Some patients may benefit from psychodynamic-oriented psychotherapy, especially if PTSD was caused by early sexual or physical abuse.
Flooding, a technique involving prolonged exposure to the adverse stimuli, has been used with some success on veterans.
In a recent study of service members with PTSD caused by the traumatic events of September 11, 2001 or Operation Iraqi Freedom, self-managed, Internet-based cognitive behavior therapy led to a greater reduction in PTSD symptoms than Internet-based supportive counseling.22
Other specific techniques used to process traumatic events include eye movement desensitization and reprocessing and hypnosis. Eye movement desensitization and reprocessing has been successful in helping the survivors of various traumas, such as domestic violence, sexual abuse, crime, and combat. The method involves psychotherapy that combines various therapeutic approaches with eye movements (or other types of rhythmical stimulation) to stimulate the brain's information-processing mechanisms.
Inpatient care is necessary only if the patient becomes suicidal or because of the presence of complicating comorbid conditions that may require inpatient treatment (eg, depression, substance abuse). Hospitalization is also indicated if the patient becomes homicidal.
Medication
Many different drugs have been used to treat specific symptoms of PTSD, such as benzodiazepines for anxiety, anticonvulsants for impulsivity and emotional lability, and clonidine for nightmares. However, the principal agents of treatment have been the various antidepressants and beta-blockers. Most medication trials on PTSD have involved male combat veterans. Results of studies on civilians show fluoxetine to be effective.23 Some studies suggest that fluoxetine demonstrates some efficacy for all 3 symptom clusters. Recently, atypical antipsychotics have been used for patients who do not respond to antidepressants.24 Patients with severe PTSD symptoms are likely to need longer treatment to experience beneficial results of taking these medications.25
Novel pilot studies in combat veterans suggest alpha-1 antagonist have efficacy on the sleep-associated symptoms of PTSD.13 Alpha-1 antagonist have not been FDA-approved for this indication; however, low-dose glucocorticoids may have a role in decreasing recall of traumatic memories, but further research is warranted.4
Recent small, double-blind, placebo controlled studies reveal that a nighttime dose of prazosin (10-15 mg) decreases nightmares and sleep disturbances in combat veterans with PTSD and increases normal dreaming patterns. Additional pilot trials reveal a mid-morning dose of prazosin also helps decrease daytime PTSD symptoms in civilian and military patients.13 However, larger randomized, placebo-controlled trials are needed to confirm these results.
Selective serotonin reuptake inhibitors
Most recent findings with SSRIs and related compounds indicate a more positive outlook for pharmacological treatment than had been suggested in earlier trials.23,16
Sertraline (Zoloft)
First drug approved by FDA for PTSD. May be effective in reducing some symptoms in at least some patients. May be particularly useful in treatment of women who have experienced sexual or physical assaults.
DosingInteractionsContraindicationsPrecautionsAdult
50-200 mg PO qd
Pediatric
Not established
DosingInteractionsContraindicationsPrecautionsIncreases toxicity of MAOIs, diazepam, tolbutamide, and warfarin, probably because of inhibition of cytochrome P-450 enzymes or displacement from plasma protein binding
DosingInteractionsContraindicationsPrecautionsDocumented hypersensitivity
DosingInteractionsContraindicationsPrecautionsPregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in preexisting seizure disorders, recent myocardial infarction, unstable heart disease, and hepatic or renal impairment
Paroxetine (Paxil)
Approved by FDA for this disorder. Studies have shown therapeutic effect on the 3 symptom clusters of PTSD, causing reduction in reexperiencing, numbing/avoidance, and hyperarousal.
DosingInteractionsContraindicationsPrecautionsAdult
Recommended starting dose: 20 mg/d PO; if indicated, may be increased in 10-mg increments at intervals >1 wk; doses from 20-50 mg are effective
Pediatric
Not established
DosingInteractionsContraindicationsPrecautionsAvoid alcohol, tryptophan, and thioridazine; avoid within 14 d of MAOIs; may inhibit metabolism of TCAs; may change concentrations with plasma-bound drugs; hyperreflexia, weakness, and incoordination have been reported with sumatriptan; monitor theophylline; caution with lithium, digoxin, diuretics, cimetidine, phenobarbital, warfarin, phenytoin, quinidine, and drugs metabolized by CYP-450 2D6 (eg, type 1C antiarrhythmics, phenothiazines, antidepressants)
DosingInteractionsContraindicationsPrecautionsConcomitant MAOIs or thioridazine
DosingInteractionsContraindicationsPrecautionsPregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in history of seizures, mania, renal disease, and cardiac disease; the CR product should not exceed 50 mg/d for elderly, debilitated, or severely renally or hepatically impaired persons
Fluoxetine (Prozac)
Recent studies have shown this drug to be superior for measures of PTSD severity, disability, and high end-state function.
DosingInteractionsContraindicationsPrecautionsAdult
20 mg PO qd/bid; not to exceed 80 mg/d
Pediatric
Not established
DosingInteractionsContraindicationsPrecautionsIncreases toxicity of diazepam and trazodone by decreasing clearance through inhibition of cytochrome P-450 enzymes; increases toxicity of highly protein–bound drugs; with MAOIs, can cause serotonin syndrome with delirium, fever, shivering, and myoclonus
DosingInteractionsContraindicationsPrecautionsDocumented hypersensitivity; concurrent MAOIs or MAOIs in previous 2 wk
DosingInteractionsContraindicationsPrecautionsPregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating therapy
Monoamine oxidase inhibitors
Have been involved in a few controlled medication trials for PTSD. In one trial, phenelzine significantly reduced intrusion (reexperiencing) symptoms but had no effect on avoidance.
Phenelzine (Nardil)
In one double-blind placebo-controlled trial, was more efficient in reducing intrusion symptoms. Has demonstrated clear superiority over placebo in double-blind trials for treating specific symptoms of panic disorders. Usually reserved for patients who do not tolerate or respond to traditional cyclic or second-generation antidepressants.
DosingInteractionsContraindicationsPrecautionsAdult
Usual starting dose: 1 tab (15 mg) PO tid; lower starting doses are advised in patients sensitive to medications (ie, the 7% of the population who are slow metabolizers)
Pediatric
Not established
DosingInteractionsContraindicationsPrecautionsCoadministration with foods containing tyramine can increase blood pressure; concurrent use with tryptophan should be approached with caution because serotonin syndrome may result; may enhance therapeutic and toxic response of meperidine, and concomitant administration of these drugs should be avoided
DosingInteractionsContraindicationsPrecautionsDocumented hypersensitivity; alcoholism, congestive heart failure, and pheochromocytoma
DosingInteractionsContraindicationsPrecautionsPregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Closely monitor for symptoms of postural hypotension; because of effect on convulsion threshold, adequate precautions should be taken when treating patients with epilepsy
Beta-blockers
Useful in controlling some symptoms of PTSD caused by hyperarousal. A recent pilot study revealed propranolol is effective in decreasing physiological signs of hyperarousal for up to 1 week when used shortly after patients with PTSD reexperience their traumatic event.26 Ideally, propranolol is to be used within 6 hours of the initial traumatic event, well before a diagnosis of PTSD is made. Larger randomized, placebo-controlled studies are warranted to confirm these findings.
Propranolol (Inderal, Betachron E-R)
Relieves exaggerated startle response, explosiveness, nightmares, and intrusive reexperiencing in some patients.
DosingInteractionsContraindicationsPrecautionsAdult
40-80 mg PO qd in divided doses; may increase up to 120-160 mg qd for optimal effects
Pediatric
Not established
DosingInteractionsContraindicationsPrecautionsCoadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase
DosingInteractionsContraindicationsPrecautionsDocumented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
DosingInteractionsContraindicationsPrecautionsPregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely
Follow-up
Further Inpatient Care
Although limited to 5 case management studies, the treatment of patients who came with PTSD symptoms after returning from Global War on Terror (GWOT) missions was examined at a center. Treatment cocktails included aripiprazole and either cognitive-behavioral psychotherapy or sertraline. The therapeutic cocktail was observed to reduce the recurrence of hyperarousal episodes, which was the predominant symptom. However, in one patient, a paradoxical hyperarousal was observed.24
Inpatient care is necessary only if the patient becomes suicidal or because of the presence of complicating comorbid conditions that may require inpatient treatment (eg, depression, substance abuse). Hospitalization is also indicated if the patient becomes homicidal.
Further Outpatient Care
Having experienced trauma, some patients with PTSD may be socially uncomfortable. Encouragement over time may be helpful to keep them therapeutically engaged, which yields optimal medical and psychiatric benefit.
Complications
Individuals with PTSD may be at increased risk for panic disorder, agoraphobia, obsessive-compulsive disorder, social phobia, specific phobia, major depressive disorder, and somatization disorder.
In one study, the relationship between the endogenous opiate system and PTSD was examined. In the study, 78 out of the 173 African American outpatient mental health patients were diagnosed with PTSD. Although the study had quite a few limitations, they noticed that there was an increased use of analgesic medications (both opiate and nonopiate) among this patient population.27
Comorbidities: Over time, untreated and undertreated individuals with PTSD are especially susceptible to a deterioration of personal and work relationships and to the development of substance abuse or dependence.
In one study, men with PTSD reported an earlier age of onset of alcohol dependence, greater alcohol use intensity and craving, and more severe legal problems due to alcohol use. Women reported greater exposure to sexually related traumas, greater frequency and intensity of avoidance of trauma-related thoughts and feelings, and greater social impairment due to PTSD. Women had higher rates of other anxiety disorders and of positive test results for cocaine use at treatment entry than men. PTSD more often preceded alcohol dependence in women than men. These findings illustrate the possibility of sex differences in the pathology of PTSD.28
Another study found that 51.9% of men with PTSD also concomitantly abused or were dependent on alcohol, while 48.5% of women with PTSD also had major depressive disorder.
Prognosis
Prognosis is difficult to determine because it varies significantly from patient to patient. Some individuals who do not receive care gradually recover over a period of years. Many individuals who receive appropriate medical and psychiatric care recover completely (or nearly completely). Rarely, even with intensive intervention, individuals experience worsening symptoms and kill themselves. In patients with PTSD who are receiving treatment, the average duration of symptoms is 36 months, compared with 64 months for those patients who do not receive treatment.
More than one third of patients who have PTSD never fully recover.
Factors associated with a good prognosis include rapid engagement of treatment, early and ongoing social support, avoidance of retraumatization, positive premorbid function, and an absence of other psychiatric disorders or substance abuse.
A recent pilot study in civilians suggests that patients who experience peritraumatic tonic immobility during the traumatic event have a poor response to pharmacologic treatment.29
A recent study has associated PTSD with a risk of developing dementia among older US male veterans. In a group of male veteran participants, those diagnosed with PTSD were twice as likely to develop dementia than those without PTSD. Discovering the biological link between these disorders would be monumental in the fight to find ways to reduce the occurrence of dementia in PTSD victims.30
Remission criteria involve subjective goals and objective goals.31 Objective goals include test results. Tests include the Treatment Outcome PTSD Scale or TOPS-832 , the Hamilton Rating Scale for Anxiety or HAM-A33 , the Hamilton Rating Scale for Depression or HAM-D34 , and the Sheehan Disability Scale35 . Criteria are as follows:
Subjective goal - No or minimal PTSD symptoms
Objective goal - TOPS-8 score less than or equal 5 or 6
Subjective goal - No or minimal anxiety
Objective goal - HAM-A score less than or equal 7-10
Subjective goal - No functional impairment
Objective goal - Sheehan Disability Scale score less than or equal to 1 on each item (mildly disabled)
Subjective goal - No or minimal symptoms of depression
Objective goal - HAM-D score less than or equal to 7
Patient Education
When a family member is diagnosed with PTSD, the entire family may be affected. Members may experience shock, fear, anger, and pain because of their concern for the victim. Living with family members who have PTSD does not cause PTSD. Yet, it can cause some similar symptoms, such as feelings of alienation from and anger toward the victim. Other family members may find it difficult to communicate with a person with PTSD. Sleep disturbance and abuse (physical and substance) may occur among family members.
Families should engage in counseling if anger, addiction, or problems in school or work become issues. Stress and anger management and couples' therapy are possibilities. Families should try to maintain their outside relationships and should continue to be involved in pleasurable activities.
For excellent patient education resources, visit eMedicine's Mental Health and Behavior Center. Also, see eMedicine's patient education articles Post-traumatic Stress Disorder (PTSD) and Stress.
The following Web sites also provide valuable information for patients and their families: US Department of Veteran Affairs National Center for PTSD, US Army Office of Behavioral Health, Afterdeployment.org, National Institute of Mental Health, American Academy of Child and Adolescent Psychiatry, and Mayo Clinic.
Miscellaneous
Medicolegal Pitfalls
One major reason for litigation in the event of trauma and criminal offenses is to punish persons involved in violence and criminal activity. As a witness to an act of violence, the victim has an obligation to report the crime and to cooperate with law enforcement officials.
This may involve testifying before a grand jury, which occurs before the case formally begins.
The victim acts as a witness to the case and, therefore, is not a party to the criminal proceedings and is not represented. This can be difficult after experiencing the event itself, which characterizes loss of power, control, and dignity.
Victims often require the support and advocacy of legal representation, but the system does not provide it. The prosecuting attorney is the supposed advocate for the victim, but the attorney's job of defending the interests of justice may conflict with the interests of the victim.
The process of a trial can be very traumatic for the victim, particularly in cases of sexual trauma. Defense tactics sometimes involve blaming the victim for the crime by tainting his or her character; this may add more pain to an already painful process.
Special Concerns
Individuals who have emigrated from countries experiencing political unrest may be unwilling to discuss their traumatic experiences because of legal issues.
A review of PTSD trials in refugees suggests PTSD may be a culture-specific diagnosis.3 Care must be taken by a health care professional when applying this diagnosis to people from nonwestern cultures where the diagnosis has not been validated, and standard PTSD assessments have not been adapted to express nonwestern concepts of disorder and idioms of distress.
In Iraq and Afghanistan war veterans, problems with anger and perceived control of violent behavior appear to be related to the hyperarousal symptoms of PTSD. This may have treatment implications, such as focusing on reduction of these symptoms.36
Acknowledgments Multimedia
(Enlarge Image) Media file 1: Brain structures involved in dealing with fear and stress.
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Brain structures involved in dealing with fear and stress.
