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Seedat in his article published in the South African Journal of Psychiatry throws light on the complications and treatment of Post Traumatic Stress Disorder. As per Seedat, Post Traumatic Stress Disorder happens to be one of the most pervasive anxiety disorders. This disorder…
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Post Traumatic Stress Disorder Psychology of the June 17, Post Traumatic Stress Disorder. S. Seedat in his article published in the South African Journal of Psychiatry throws light on the complications and treatment of Post Traumatic Stress Disorder. As per Seedat, Post Traumatic Stress Disorder happens to be one of the most pervasive anxiety disorders. This disorder pertains to the evincing of a pathological response as a consequence of exposure to a traumatic event. This includes nightmares, a tendency on the part of the patient to avoid stimuli associated with the traumatic event, psychological distress, enhanced arousal, negative cognition and mood alterations.

Studies have shown that symptoms of PTSD appear shortly after the traumatic event and may subside in many patients. However these symptoms may persist in nearly forty percent of the patients as chronic PTSD. The sad thing is that many cases of PTSD go undiagnosed. The treatment goals in the case of PTSD pertain to reducing the severity of symptoms, decreasing the functional impairment owing to PTSD, avoiding relapse, and bettering the overall quality of life of the patients. The treatment of PTSD involves both pharmacological and non-pharmacological treatment.

Keeping in view the complications associated with pregnancy and lactation, the risk of treating pregnant and lactating patients needs to be weighed against the risk associated with denying the treatment. The assessment and treatment of PTSD may pose many challenges for the mental healthcare professionals treating children and the elderly. Success in the treatment of PTSD greatly depends on an early diagnosis and treatment. Summarized ArticleSeedat, S. (2013). Post-Traumatic Stress Disorder.

South African Journal of Psychiatry, 19(3), 187-207. Post-Traumatic Stress DisorderSeedat, S., South African Journal of Psychiatry1. IntroductionPost-traumatic stress disorder (PTSD) is among the most prevalent anxiety disorders, both interms of lifetime and 12-month prevalence rates documented in epidemiological studiesworldwide. The National Comorbidity Survey Replication (NCS-R) study conducted in theUSA, for example, found the lifetime prevalence of PTSD to be 6.

8% while the 12-monthprevalence was 3.5%. [1,2] The South African Stress and Health Study (SASH) documentedlower lifetime (2.3%) and 12-month (0.6%) rates, although PTSD was among the anxietydisorders with the highest proportion of severe cases (36% of all individuals diagnosed withPTSD were severely ill). [3] High rates of PTSD (19.9%) have also been documented amongSouth African patients attending primary healthcare clinics. [4]2. Diagnosis and clinical characteristicsThe disorder represents a pathological response to a traumatic event, characterised bysymptoms of recurrent and intrusive distressing recollections of the event (e.g. nightmares, asense of reliving the experience with illusions, hallucinations, or dissociative flashbackepisodes, intense psychological or physiological distress at exposure to cues that resemble thetraumatic event); avoidance of stimuli associated with the trauma (e.g. inability to recallimportant aspects of the trauma, loss of interest, estrangement from others); and increasedarousal (sleep disturbances, irritability, difficulty concentrating, hypervigilance, andexaggerated startle response).

 [5] These symptoms cut across three recognised symptomclusters (re-experiencing, avoidance or numbing and hyperarousal), produce distress andimpairment for individuals, and form the essential targets for treatment. The Diagnositic andStatistical Manual of Mental Disorders, Fifth Edition (DSM-V) includes an additional clusterof symptoms characterised by negative alterations in cognition and mood. The full symptompicture must be present for more than 1 month for the diagnosis to be made.

 [6] PTSD isclassified in the category of trauma- and stressor-related disorders, and separate from theanxiety disorders, in the DSM-V. Risk factors that increase the likelihood of PTSD includeseverity of the traumatic exposure, history of past trauma or previous psychiatric disorder,female gender, experience of further stressful events and lack of social support.3. AssessmentAs a general rule, a comprehensive review of the differential diagnosis of the anxietysymptoms should be done, ruling out or treating other psychiatric diagnoses and medicalcauses.

 Thus, as part of the initial diagnostic assessment, and after each subsequent treatmenttrial, should response to treatment be unsatisfactory, it is important to evaluate symptomsassociated with PTSD (e.g. insomnia, aggression, nightmares, suicidality, psychoticsymptoms). Other considerations include comorbid diagnoses (including depression, otheranxiety disorders, substance abuse, bipolar disorder), other issues such as concurrent medicalillness especially that which may be undiagnosed (e.g. thyroid disease), ongoing trauma, andlegal/compensation issues, ongoing use of anxiety-producing substances (e.g. caffeine, otherstimulants), pregnancy, and poor adherence to treatment.

 [7] Those with PTSD, with andwithout depression, are at increased risk for suicidality, and it is important to assess suiciderisk both at the initial evaluation and subsequent follow-up visits. [7]Longitudinal studies indicate that PTSD is a disorder of chronicity in that symptoms appearshortly after the traumatic event, subside in many individuals, but can persist in as many as40% in the form of chronic PTSD. [5] Given that a significant number of cases of PTSD areundiagnosed and undertreated, it is important to inquire about exposure to trauma, and tomaintain a high index of suspicion and a high level of awareness of the disorder.

 Patients withPTSD are frequent users of general medical and psychiatric services, have high rates ofcoexisting psychiatric (e.g. major depressive disorder, alcohol and drug use disorders, otheranxiety disorders) and medical conditions (e.g. asthma, gastrointestinal disorders), and, asalready mentioned, are at a high risk for suicide attempts. [8,9] These comorbid diagnosesmay complicate proper diagnosis and alter the course of treatment.

 The disorder is also highlyreactive to environmental reminders of the traumatic event and to subsequent stressful lifeevents and can therefore have a fluctuating course.4. Treatment4.1 Treatment goals in PTSDThere are several specific goals of treatment that should all be borne in mind: reducingsymptom severity; preventing the occurrence of, and/ or treating, comorbid disorders;decreasing functional impairment; modifying pathogenic fear schemas; building resilience;preventing relapse; and improving quality of life of patients.

 [10] The most commondefinitions of treatment response in PTSD patients are a decrease of 30% or more [11] in theClinician Administered PTSD Scale (CAPS) score [12] or a score of 1 (very much) or 2 (muchimproved) [13] in the Clinical Global Impressions Scale-Improvement item (CGI-I). [14]4.2 General aspects of treatmentThe treatment of PTSD has been the subject of several recent meta-analyses and systematicreviews. Several treatment guidelines are available and these together have informed thetreatment guideline that is recommended here.

 They include guidelines from the WorldFederation of Societies of Biological Psychiatry, [15] the US Institute of Medicine (IOM), [16]the American Psychiatric Association, [17] the UK National Institute of Clinical Excellence(NICE), [18] the Australian National Centre for PTSD, [19] the British Association forPsychopharmacology, [20] and the International Psychopharmacology Algorithm Project(IPAP). [7] All of these guidelines acknowledge that there are two distinct approaches that areof proven benefit in PTSD: pharmacological and psychotherapeutic.

 Therefore, the first choiceto be made is whether to offer medication, psychotherapy, or both. Psychotherapeutictreatments, if not used initially, can be added to, or replace pharmacotherapy.Chronic PTSD is defined as PTSD of more than 3 months duration. Most treatment guidelinesrecommend the use of either selective serotonin reuptake inhibitors (SSRIs) or exposure-based, traumafocused cognitive-behaviour therapy (TF-CBT) as first-line therapy.

 However, itshould be mentioned that both the US IOM guidelines [16] and the UK NICE guidelines[18] onthe sum of data suggest that evidence for the efficacy of pharmacological therapies, namelySSRIs, is at best tentative. The NICE guidelines, [18] for example, do not recommend drugtreatments as a routine first line for adults with PTSD (for prescription either by a generalpractitioner or psychiatrist), but rather advocate for the use of TF-CBT.4.3 Acute treatmentAn adequate trial requires 6-12 weeks, but the clinician should expect some response after 4-6weeks with adequate dosage.

 A minimum course of exposure-based, TF-CBT is 8-12 weekly orbiweekly sessions for exposure to a single-incident trauma. More sessions may be required ininstances of multiple traumatic exposures or the presence of comorbidity.4.4 Maintenance treatmentPTSD is a disorder that is characterised by symptom persistence and long-term treatment forat least 12-24 months is recommended. The SSRIs and the serotonin-norepinephrine reuptakeinhibitor (SNRI), venlafaxine, have demonstrated long-term efficacy.4.5 Pharmacological treatmentThe SSRIs and SNRIs are the two groups of antidepressants that have, to date, been the mostrigorously studied in placebo-controlled randomised controlled trials (RCTs) and areconsidered as first-line agents for PTSD.

 Long-term efficacy (treatment for at least 12-24months) has also been demonstrated with both classes of agents. [15]Of the SSRIs, paroxetine, sertraline and fluoxetine currently have the best evidence forefficacy.[7,15-17] Paroxetine and sertraline are the only two that are US Food and DrugAdministration (FDA) indicated for PTSD. In a meta-analysis of 35 RCTs (of 14 weeks or lessin duration) involving a total of 4 597 participants, evidence for efficacy was most convincingfor the SSRIs, across all symptom clusters and for co-occurring depression and disability.

 [13]However, the SSRIs as a class seem to be less effective in combat-related PTSD than in non-combat-related PTSD. [17] Even when treated with this class of agents, response rates inPTSD rarely exceed 60% after a first trial of medication and less than 20-30% of patientsachieve full remission. [7,15-17] This suggests that currently available, efficacious agents stillfall short of the ideal because of limited response and remission rates, and tolerability issues.4.6 Non-pharmacological treatmentThere are now more than 50 published RCTs examining the efficacy of CBT for PTSD.

 [20]TF-CBT has the best established research base of well-designed RCTs. Prolonged exposure hasbeen found to be highly effective in the treatment of women with PTSD following sexual orphysical assault. A minimum course of 8-12 weekly or biweekly sessions is recommended.The components of CBT associated with the largest treatment effects are cognitive therapy(CT) and prolonged exposure; they have been shown to be superior to waitlist, supportivecounselling, non-specific therapies; and treatment as usual.

 [21] Eye movementdesensitisation and reprocessing (EMDR) which combines imaginal exposure with lateral eyemovements, like exposure and CT, also has established efficacy, but critics of this procedurecite poor methodological quality and evidence that the procedural component, which ispurported to differentiate it from exposure, is in fact inactive. [22] A recent Cochrane review[22] concluded that EMDR was more effective than traditional therapies or no therapy but notdifferent from CBT and stress management.

 The IOM found the quality of the body of evidencefor EMDR to be too low to inform conclusions regarding treatment efficacy. [16]4.7 Special populations4.7.1 Pregnancy and lactationThe risks of drug treatment during pregnancy need to be weighed against the risks ofwithholding treatment for PTSD. During the first trimester, SSRIs do not increase the risk ofbirth defects; the exception to this is paroxetine, which is associated with a 1.

5-fold increasedrisk of congenital heart defects. [23] Clinical guidelines recommend that paroxetine bediscontinued during pregnancy. SSRIs taken after 20 weeks gestation may be associated withan increased risk of persistent pulmonary hypertension in the neonate, and all antidepressantsadministered in the third trimester may cause discontinuation effects (e.g. increased muscletone, irritability, disrupted sleep, jitteriness) although these tend to be mild and self-limiting.

Newer antidepressants, such as venlafaxine, have been associated with poor neonataladaptation syndrome (tremors, irritability, shivering, feeding disturbances, increased muscletone, respiratory difficulties) although it is unclear whether this is the result of medicationwithdrawal or toxicity. Treatment is supportive and symptoms usually resolve within 2 weeks.Tricyclic antidepressants (TCAs) are regarded as relatively safe in pregnancy although there isan increased risk of preterm delivery compared with SSRIs or no antidepressants.

Desipramine is the preferred TCA during pregnancy owing to its relatively weakanticholinergic effects. [24] Lithium (Ebsteins anomaly) and antiepileptic medications suchas carbamazepine (neural tube defects, craniofacial defects, cardiac malformations) andvalproate (neural tube defects, spina bifida, pulmonary atresia) carry an increased risk ofbirth defects. To date, lamotrigine has not been associated with intrauterine growth defects orneurobehavioural toxicity.

 No significant risk of teratogenicity with the older atypicalantipsychotics (olanzapine, risperidone, quetiapine) has been documented. However, theaforementioned antipsychotics are associated with maternal hyperglycaemia, impairedglucose tolerance and weight gain which could contribute to maternal complications duringpregnancy. [24] Newer atypical antipsychotics (e.g. aripiprazole, ziprasidone) have beenassociated with delays in skeletal ossifications, increased fetal weight and fetal mortality.

Long-term safety data on the use of antidepressants in pregnancy are lacking. Importantfactors to consider include the time between medication administration and feeding, andinfant size and infant metabolism. Most SSRIs do not attain detectable levels in breast milkand are not associated with disturbed infant development or neuropathology. Sertraline andparoxetine may be good choices for lactating women as these SSRIs have specifically beenassociated with undetectable levels in infants.

 TCAs have been associated with few adverseeffects in breastfed infants, while newer antidepressants such as venlafaxine and mirtazapineare considered to be moderately safe.4.7.2 Children and adolescentsYoung children with PTSD, rather than reliving the trauma through repeated intrusivememories, may re-experience the trauma through repetitive play. Avoidance phenomena mayalso be more difficult to elicit in very young children who may struggle to verbalise theirexperiences.

 In addition to PTSD and acute stress disorder (ASD), traumatised children andadolescents may have a broad range of other psychopathological outcomes, in particular moodand anxiety disorders, behavioural disorders (e.g. attention-deficit hyperactivity disorder,conduct disorder), and substance use disorders. As with adults, interventions comprisingpsychotherapy (e.g. TF-CBT, family therapy) and pharmacotherapy (e.g. SSRIs, alpha-adrenergic agonists) are used.

 Practice parameters developed by the American Academy ofChild and Adolescent Psychiatry [25] recommend that the treatment of mild PTSD begin withTF-CBT. Treatment studies suggest 12 sessions of TF-CBT where PTSD is uncomplicated, buta number of children and adolescents may require longer-term treatment. Currently little isknown about the effectiveness of pharmacotherapeutic agents in paediatric PTSD as therehave been few controlled studies of SSRIs.

 Children and adolescents with more severe PTSDand with comorbid mood and anxiety disorders are likely to benefit from an SSRI. [25]4.7.3 The elderlyThe assessment and treatment of PTSD may pose challenges for psychiatrists involved intreating PTSD in older adults. Specific symptom profiles may differ in the older adult,particularly in those individuals with chronic PTSD. Distress when exposed to traumarelatedcues appears to be potentially salient and it is possible that this symptom motivates otherfeatures of PTSD in older adults, such as avoidance and emotional numbing.

 [26] Thisconstellation of symptoms may lead to misdiagnosis, for example, major depression ordysthymic disorder. Several factors should be considered when selecting a medication for anolder patient with PTSD. These include prior treatment response, target symptoms,concurrent physical illness and medications, and drug tolerability. In order to reach theoptimal dose for an older patient without causing intolerable sideeffects, it is well worthremembering the adage start low and go slow.

 Important considerations in pharmacologicaltreatment also include the heightened sensitivity for anticholinergic drug effects, increasedsensitivity for extrapyramidal symptoms, an increased risk for orthostatic hypotension andelectrocardiograph changes, and the possibility of paradoxical reactions (e.g. aggression) tobenzodiazepines. SSRIs have been shown to be relatively safe in the elderly and are generallybetter tolerated than TCAs. Recommended doses of SSRIs for PTSD are the same as foryounger adults.

 However, the potential for SSRIs to cause gastrointestinal and other bleeds,hyponatraemia, postural hypotension, and falls needs to be borne in mind in this age group.4.8 Managing partial and non-respondersSee steps 3 and 4 of algorithm below.4.9 Algorithm Step 1. Initiating treatmentThe starting dose can be low (fluoxetine 10-20 mg; sertraline 25-50 mg; paroxetine, 10-20mg; venlafaxine 37.5-75 mg). Other SSRIs include citalopram (10-20 mg), fluvoxamine (25-50mg) and escitalopram (5-10 mg), for which there is less evidence.

 Based on currently availabledata for the SSRIs and SNRIs, statistically and clinically significant improvement is often seenby weeks 2 to 4. An adequate trial typically requires 6-12 weeks at an adequate dosage (e.g.fluoxetine 20-40 mg; sertraline 50-100 mg; paroxetine 20-40 mg), but some response shouldbe expected after 4-6 weeks. [7]Other antidepressant options for which there is less robust evidence include mirtazapine,bupropion, and nefazodone.

 The older antidepressants, such as TCAs, e.g. amitriptyline,imipramine and the monoamine oxisase inhibitors (MAOIs, e.g. phenelzine) havedemonstrated efficacy in placebo-controlled studies that have primarily included individualswith combat-related PTSD. In light of the safety profiles and concerns of toxicity with theseagents (cardiotoxicity, seizure risk, and anticholinergic effects with the TCAs, and dietaryrestrictions and risk of hypertensive crisis with the MAOIs), they should preferably not beused as a first or second choice.

 [7,15-17] Table 1 lists recommended drug doses. [15]Step 2. Maintaining a responseIt is important to note that while many patients will experience symptom improvement within12 weeks with at least a 50% reduction in PTSD symptoms, further improvement in coresymptoms, disability, and overall functioning often occurs with continued treatment. If apatient is adequately responsive (at least a 50% improvement) after 12 weeks of treatment anddemonstrates no intolerance, medication should be continued for at least 1-2 years .Step 3. Managing partial responseIf the patient is only partially responsive to the first trial of medication (25-50% or morereduction in symptoms), it is prudent firstly to optimise the dose of medication (i.e. titrate upto the maximum allowed or tolerated dose).

 Before doing this, it is important to reassess forpersisting core PTSD symptoms (intrusion, avoidance, numbing, and hyperarousal), sleepdisturbances, other PTSD symptoms (e.g. irritability, hostility, aggression, panic, psychoticsymptoms), bipolar spectrum disorder, and substance abuse. [7]These ongoing symptoms can be saliently targeted through augmentation strategies althoughit must be noted that the evidence-base for augmentation strategies is limited.

 For example,olanzapine and risperidone (for which there is double-blind, placebo-controlled evidence forefficacy) can be used to target associated psychotic symptoms (e.g. paranoid ideation), andaggression. It is important to mention that since augmentation studies of antipsychotics wereessentially short-term trials, the possibility of occurrence of severe adverse effects (viz.metabolic effects, cardiac effects, tardive dyskinesia) remain a concern.

 Anticonvulsants (e.g.valproate, lamotrigine, carbamazepine, topiramate), given their well-known anti-kindlingproperties, may also be effective as augmentation for symptoms of irritability, impulsivity,labile mood, and anxiety, while alpha-1 inhibiting agents (e.g. prazosin, guanfacine) haveshown promise in the treatment of nightmares, insomnia and other sleep-related disturbancesin PTSD. [27] Hypotension, syncope and tachycardia are potential side-effects with prazosin;hence medical history, risks of hypotension and blood pressure monitoring should beconsidered.

 No data exist on the efficacy of benzodiazepines as augmentation treatment,although there are some data indicating their lack of efficacy as monotherapy (e.g.alprazolam) in chronic PTSD. [28]Exposure-based, TF-CBT (8-12 sessions) may also be considered as an augmentation strategyat this point. However, there are currently no published controlled studies of combinedpharmacotherapy and psychotherapy in PTSD.Step 4. Managing non-responseIf there is no response (i.e. less than 25% improvement) to an SSRI and core PTSD symptomspersist after 4-6 weeks of an adequate medication dose (e.g. fluoxetine 40 mg/day, sertraline150 mg/day), then it is advisable to switch to another SSRI, SNRI, or noradrenaline andspecific serotonergic antidepressant (NaSSA) such as mirtazapine, bupropion; or alternativelyto augment the same medication with another agent.

 The choice of an augmentation agentwill depend on the presence of comorbid disorders; for example, the presence of a comorbidanxiety or mood disorder would probably necessitate the utilisation of an agent (e.g.antidepressant) that is effective for both PTSD and that disorder. [20] It is not known whethera sequential trial of a second SSRI is as effective as switching to an SNRI or NaSSA after thefirst unsuccessful SSRI trial.

 [20] If there is still no response after 6-12 weeks, then it isrecommended that one add an atypical antipsychotic, anticonvulsant, a TCA, or CBT. If thepatient fails on all of the above, it is essential at this point to re-evaluate the diagnosis and toconsider switching (e.g. to a TCA or MAOI if these have not been tried already) or to add athird medication.4.10 Early interventions for PTSDTF-CBT is the only early intervention (i.e. given 1-3 months after trauma) that at the presenttime has convincing evidence of efficacy in ASD and acute PTSD.

 [20] There is no goodevidence that psychological interventions (i.e. psychological debriefing), either single ormultiple sessions, given routinely to everyone following a traumatic exposure, irrespective ofsymptoms, work. At present there is no conclusive evidence for the use of drug treatments toprevent PTSD in the early aftermath of trauma. Benzodiazepines are frequently prescribed inthe aftermath of a traumatic event to control associated nonspecific behavioural disturbances(e.g. marked anxiety or agitation, insomnia) and/or to reduce active post-traumaticsymptoms (e.g. hypervigilance).

 However, there is no compelling scientific evidence of theeffectiveness of benzodiazepines either in the prevention of PTSD or in the treatment of corePTSD symptoms once they have developed. [22] In fact, there is evidence to indicate thatbenzodiazepines may contribute to the development and/or chronicity of PTSD symptoms.[28,29]5. Summary points* PTSD is a challenging disorder to treat.* It should be recognised that the majority of individuals with PTSD in South Africa may nothave guaranteed access to diagnostic, pharmacotherapeutic and evidence-basedpsychotherapeutic services as suggested in this guideline.

* Antidepressants (in particular SSRIs) and CBT (exposure-based, trauma-focused CBT)remain the mainstay of treatment for the disorder.* Use an SSRI or SNRI as first-line therapy and treat the patient at the maximum tolerateddose for at least 4-6 weeks before assessing responsiveness.* Once a patient has responded to drug treatment, it should be continued for at least 12-24months before considering gradual withdrawal.* Cost should be factored into the choice of medication; the most affordable medicationshould preferably be selected to allow for funding of the minimum of 1 year of suggestedpharmacotherapy.

* The minimum course of exposure-based, trauma-focused CBT is 8-12 weekly or biweeklysessions for exposure to a single-incident trauma.* In deciding on a treatment plan for the patient, it is important to consider the following atbaseline and follow-up assessments: the presence of ongoing trauma, comorbid diagnoses(both psychiatric and medical), suicidality, substance abuse, psychosis, pregnancy, treatmentcompliance, pharmacokinetic (drug-drug interaction) issues, and legal or compensationissues.

* There is no evidence for the efficacy of systematic, brief, single-session interventions (i.e.debriefing) focusing on the traumatic incident. However, providing general practical andsocial support and guidance to anyone following a traumatic incident is recommended.* The quest to investigate novel pharmacological agents (e.g. D-cycloserine, a partial agonistof N-methyl-D-aspartate (NMDA) receptor through its mechanism on fear extinction) andtherapeutic strategies (e.g. virtual reality exposure therapy), for the management of PTSDremains an ongoing pursuit.

* Several other novel agents (e.g. propranolol, hydrocortisone) have been investigated in theprevention of PTSD (i.e. as prophylaxis) with mixed results. Currently SSRIs are beinginvestigated in placebo-controlled trials as an early intervention in ASD to prevent the laterdevelopment of PTSD. However, there is insufficient evidence to recommend the use of any ofthese agents.References[1.] Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributionsof DSM-IV disorders in the National Comorbidity Survey Replication.

 Arch Gen Psychiatry2005;62:593-602. [http://dx.doi.org/10.1001/archpsyc.62.6.593][2.] Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-monthDSMIV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry2005;62:617627. [http://dx.doi.org/10.1001/archpsyc.62.6.617][3.] Herman AA, Stein DJ, Seedat S, et al. The South African Stress and Health (SASH) study:12-month and lifetime prevalence of common mental disorders.

 S Afr Med J 2009;99:339-344.[4.] Carey PD, Stein DJ, Zungu-Dirwayi N, Seedat S. Trauma and posttraumatic stressdisorder in an urban Xhosa primary care population: Prevalence, comorbidity, and service usepatterns. J Nerv Ment Dis 2003;191:230-236.[5.] American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders,Fourth Edition, Text Revision (DSM-IV-TR). Washington, DC: American PsychiatricAssociation, 2000.[6.] American Psychiatric Association.

 Diagnostic and Statistical Manual of Mental Disorders(5th ed.). Arlington, VA: American Psychiatric Association, 2013.[7.] Davidson JRT, Bernick M, Connor KM, et al. A psychopharmacology algorithm fortreating posttraumatic stress disorder. Psychiatr Ann 2005;35:887-898.[8.] Hidalgo RB, Davidson JR. Posttraumatic stress disorder: Epidemiology and health-relatedconsiderations. J Clin Psychiatry 2000;61:5-13.[9.] Nock MK, Hwang I, Sampson N, et al.

 Cross-national analysis of the associations amongmental disorders and suicidal behavior: findings from the WHO World Mental HealthSurveys. PLoS Med 2009;6:e1000123.[10.] Ursano JR, Bell C, Eth S, et al. Practice guideline for the treatment of patients with acutestress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:S3-S31.[11.] Hamner MB, Robert S, Frueh BC. Treatment-resistant posttraumatic stress disorder:Strategies for intervention.

 CNS Spectrums 2004;9:740-752.[12.] Blake DD, Weathers FW, Nagy lM. A clinical rating scale for assessing current andlifetime PTSD: The CAPS 1. Behavioral Therapy 1990;18:187-188.[13.] Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder(PTSD). Cochrane Database of Syst Revi 2006;1:CD 002795.[14.] Guy W. ECDEU Assessment Manual for Psychopharmacology. Washington, DC:Government Printing Office, 1976.[15.] Bandelow B, Zohar J, Hollander E, et al.

 World Federation of Societies of BiologicalPsychiatry (WFSBP) guidelines for the pharmacological treatment of anxiety, obsessivecompulsive and post-traumatic stress disorders-first revision. World J Biol Psychiatry2008;9:248-312. [http:// dx.doi.org/10.1080/15622970802465807][16.] Committee on Treatment of Posttraumatic Stress Disorder. Treatment of PosttraumaticStress Disorder: An Assessment of the Evidence. Washington, DC: The National AcademiesPress, 2008.[17.] Ursano RJ, Bell C, Eth S, et al.

 Practice guideline for the treatment of patients with acutestress disorder and posttraumatic stress disorder. Am J Psychiatry 2004;161:3-31.[18.] National Collaborating Centre for Mental Health. Post-traumatic Stress Disorder: TheManagement of Post-traumatic Stress Disorder in Primary and Secondary Care. London:National Institute for Health and Clinical Excellence, 2005.[19.] Forbes D, Creamer M, Phelps A, et al. Australian guidelines for the treatment of adultswith acute stress disorder and post-traumatic stress disorder.

 Aust N Z J Psychiatry2007;41:637-648.[20.] Baldwin DS, Anderson IM, Nutt DJ, et al. Evidence-based guidelines for thepharmacological treatment of anxiety disorders: Recommendations from the BritishAssociation for Psychopharmacology. J Psychopharmacol 2005;19:567-596.[21.] Watts BV, Schnurr PP, Mayo L, Young-Xu Y, Weeks WB, Friedman MJ. Meta-analysis ofthe efficacy of treatments for posttraumatic stress disorder. J Clin Psychiatry2013;74(6):e541-e550.

 [http://dx.doi.org/10.4088/JCP.12r08225][22.] Cloitre M. Effective psychotherapies for posttraumatic stress disorder: A review andcritique. CNS Spectrums 2009;14:32-43.[23.] Reid S, Barbui C. Long term treatment of depression with selective serotonin reuptakeinhibitors and newer antidepressants. BMJ 2010;340:752-756. [http://dx.doi.org/10.1136/bmj.c1468][24.] Kloos AL, Dubin-Rhodin A, Sackett JC, et al. The impact of mood disorders and theirtreatment on the pregnant woman, the fetus, and the infant.

 Curr Psychiatry Rep 2010;12:96-103. [http://dx.doi.org/10.1007/s11920-010-0098-6][25.] American Academy of Child and Adolescent Psychiatry. Practice parameters for theassessment and treatment of children and adolescents with posttraumatic stress disorder. JAm Acad Child Adolesc Psychiatry 1998;37:4S-26S.[26.] Averill PM, Beck JG. Posttraumatic stress disorder in older adults: A conceptual review.J Anxiety Disord 2000;14:133-156.[27.] Berger W, Mendlowicz MV, Marques-Portella C, et al.

 Pharmacologic alternatives toantidepressants in posttraumatic stress disorder: a systematic review. ProgNeuropsychopharmacol Biol Psychiatry 2009;33:169-180. [http://dx.doi.org/10.1016/j.pnpbp.2008.12.004][28.] Gelpin E, Bonne O, Peri T, et al. Treatment of recent trauma survivors withbenzodiazepines: A prospective study. J Clin Psychiatry 1996;57:390-394.[29.] Mellman TA, Bustamante V, David D, Fins AI. Hypnotic medication in the aftermath oftrauma.

 J Clin Psychiatry 2002;63:1183-1184.Table 1. Recommended daily drug doses for post-traumatic stressdisorder [15] *Selective serotonin reuptake inhibitors (SSRIs) Fluoxetine 20-40 mg Sertraline 50-100 mg Paroxetine 20-40 mgSerotonin-norepinephrine reuptake inhibitors (SNRI) Venlafaxine 75-300 mgNoradrenergic and specific serotonergic antidepressants (NaSSA) Mirtazapine 30-60 mgTricyclic antidepressants (TCAs) Amitriptyline 75-200 mg Imipramine 75-200 mgAtypical antipsychotics Risperidone 0.

5-6 mg Olanzapine (adjunctive) 2.5-20 mgOther agents Lamotrigine 25-500 mg Prazosin (for nightmares) 1-10 mg Phenelzine (MAOI) 45-90 mg* Reprinted with permission from Bandelow B, Zohar J, Hollander E,et al. World Federation of Societies of Biological Psychiatry(WFSBP) guidelines for the pharmacological treatment of anxiety,obsessive compulsive and post-traumatic stress disorders-firstrevision. World Journal of Biological Psychiatry 2008;9:248-312.Informa Healthcare. For educational purposes only.

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