Social Anxiety Disorder

EPIDEMIOLOGY AND CLINICAL COURSE

In the United States, the lifetime and past-year prevalence of social anxiety disorder

is approximately 13% and 7%, respectively.

14,124 The male-to-female prevalence

ratio is approximately 2:3.

9 Social anxiety disorder usually begins early in life, with

a mean onset between ages 14 and 16 years.

125 More than 50% of patients are

affected before adolescence, and a history of shyness and behavioral inhibition

throughout childhood is common.

125 Unless effectively treated, the clinical course is

often chronic, unremitting, and lifelong, and only 20% to 40% of patients are

reported to recover after 20 years of living with this condition.

124

COMORBIDITY AND CLINICAL SIGNIFICANCE

Comorbidity in social anxiety disorder is high, with an estimated 70% to 90% of

individuals having at least one other psychiatric disorder in their lifetime.

1,124,125

Common comorbid conditions include simple phobia, major depression, GAD, panic

disorder, body dysmorphic disorder, and alcohol abuse. Because of its early onset,

social anxiety disorder usually precedes the development of comorbid disorders.

Alcohol is commonly used to decrease anxiety in social situations. The risk of

suicide attempts is high, especially in those with both social anxiety disorder and

another psychiatric illness, like depression.

9

Because social anxiety disorder usually begins during the teenage years, it can

seriously interfere with development of normal social skills, achievement of full

academic and career potentials, and abilities to form interpersonal relationships.

126

This leads to functional disabilities that may persist for a lifetime. Social anxiety

disorder is associated with unemployment, lower levels of education, and

dependence on public financial support systems.

9 Persons with social anxiety

disorder are less likely to marry, and more than half report moderate-to-severe

impairments in their abilities to carry out ordinary daily activities.

126

ETIOLOGY AND PATHOPHYSIOLOGY

Social anxiety disorder is a familial disease, but the relative contributions of genetic

versus environmental influences have not been differentiated.

17 Early factors

predisposing to its development include anxious behavior modeling in parents and

parental overprotection.

1 Shyness in children, which is associated with later

development of social anxiety disorder, has been linked to a specific genetic

polymorphism of the serotonin transporter promoter region.

127

Biologic studies suggest performance-only social anxiety disorder has a different

underlying pathophysiology involving noradrenergic system dysfunction. Conversely,

in nonperformance-only social anxiety disorder, there is substantial evidence for

dopaminergic (decreased dopamine neurotransmission) and serotonergic dysfunction

(5-HT type-2 receptor hypersensitivity).

128–130

TREATMENT OF SOCIAL ANXIETY DISORDER

Early detection and treatment of social anxiety disorder are vital in reducing lifelong

functional consequences and may prevent development of comorbid disorders.

Because of the nature of the disorder, some sufferers are reluctant to seek treatment

resulting in an average treatment delay of 16 years.

131 Those who seek help, even in

psychiatric settings, are rarely diagnosed and treated appropriately.

125

Pharmacotherapy has become first line, but nonpharmacotherapy, particularly CBT,

is also beneficial.

20 Data do not support the routine use of combined modalities in the

management of social anxiety disorder; clinicians should determine whether

combined therapy would be useful on a case-by-case basis.

132

Selective Serotonin Reuptake Inhibitors and Serotonin and Norepinephrine

Reuptake Inhibitors

As with other anxiety disorders, SSRIs, in addition to the SNRI venlafaxine, are

considered the primary treatment option for most patients with social anxiety

disorder

125

for which paroxetine, sertraline, fluvoxamine CR, and venlafaxine XR are

FDA-approved.

132 Nonetheless, fluoxetine, citalopram, and escitalopram have also

demonstrated efficacy in controlled clinical trials although fluoxetine has negative

evidence as well.

20,132 Preliminary evidence with duloxetine suggests this agent may

be useful.

133

Unlike patients with GAD and panic disorder, those with social anxiety disorder

often tolerate standard antidepressant starting doses. Target doses for social anxiety

disorder are typically within the normal antidepressant dosage ranges. It is thought

SSRIs exhibit a flat dose–response curve.

134 Fixed-dose studies of paroxetine (20,

40, and 60 mg/day) and duloxetine (≥60 mg/day) in social anxiety disorder found no

overall difference in efficacy between doses.

133,135 Although some individuals may

require higher dosages, adequate time (2–4 weeks) should be allowed before the

dosage is increased. Response to SSRIs occurs gradually, and an adequate

medication trial to assess response should last at least 8 to 10 weeks. Many who

experience minimal response at week 8 may show a good response at week 12, and

improvements have been found to continue throughout 16 weeks of treatment.

136

Other Antidepressants

The MAOIs phenelzine (60–90 mg/day), tranylcypromine (30–60 mg/day), and

selegiline (5 mg twice daily) have also demonstrated marked efficacy for social

anxiety disorder but are reserved for SSRI nonresponders.

20,125,132

Case reports and open studies suggest bupropion may be useful in treating social

anxiety disorder, but controlled trials are needed to define its role.

125 Mirtazapine has

conflicting evidence from small RCTs but may be considered in SSRI

nonresponders.

20

Imipramine is ineffective for social anxiety disorder, and TCAs

(except clomipramine) are not among the recommended treatment options.

20,125,132

Likewise, nefazodone is not recommended given the risk of hepatotoxicity and

conflicting evidence, including one negative RCT.

20

Benzodiazepines

Benzodiazepines are generally considered second-line therapy for social anxiety

disorder, as they have limited efficacy in treating psychiatric comorbidities and

abuse/dependence potential. In clinical practice, they are commonly used in

combination with SSRI therapy on an as-needed basis before participation in

stressful social situations.

132 However, the efficacy of adjunctive benzodiazepines to

decrease time to response or increase response rate is unclear.

137 The high-potency

benzodiazepines may be useful as monotherapy in select patients. Clonazepam (1–3

mg/day) was markedly efficacious in one controlled study, whereas alprazolam (1–6

mg/day) showed only modest efficacy compared with placebo.

132

β-Blockers and Other Miscellaneous Agents

β-Adrenergic receptor blockers reduce peripheral autonomic symptoms of anxiety

and, thus, are useful for performance-related social anxiety disorder.

125 Propranolol

(10–80 mg) and atenolol (25–50 mg) are the two recommended agents and can be

used on an as-needed basis (1–2 hours before the performance) to reduce

performance

p. 1751

p. 1752

anxiety symptoms such as tremors, palpitations, and blushing. A test dose should be

tried before the actual occasion to assess tolerability.

Pregabalin is also considered to be an acceptable first-line agent, in the absence of

comorbidities which would benefit from an SSRI, based on placebo-controlled trials

for acute management and relapse prevention.

138

It appears a higher pregabalin dose

(450–600 mg/day) may be necessary for effective treatment. Other anticonvulsants,

antipsychotics, and miscellaneous agents have also been reported to be effective in

the treatment of social anxiety disorder, but they are considered second- or third-line

treatments.

20,43,132 These include gabapentin, tiagabine, topiramate, valproate

derivatives, olanzapine monotherapy, adjunctive aripiprazole, adjunctive

risperidone, and atomoxetine.

Nonpharmacologic Treatments

Several studies have demonstrated CBT to be comparable to medications in the

treatment of social anxiety disorder.

139 Although medications may work faster, CBT

is believed to result in longer-lasting treatment gains with effects persisting for 1 to 5

years. The cognitive therapy component changes maladaptive thought patterns, such

as expectations of performing poorly and over concern about negative evaluation by

others.

139 The behavioral therapy component, as in other anxiety disorders, involves

repeated exposure and practice performing in those feared situations. Social skills

training can also be beneficial in improving interpersonal communication skills.

CLINICAL PRESENTATION OF SOCIAL ANXIETY DISORDER

CASE 83-8

QUESTION 1: S.H., an 18-year-old man, is brought for psychiatric consultation by his mother who complains

her son is extremely shy and she’s concerned about his ability to “fit in” at college. S.H. was referred to the

psychiatrist by his primary-care physician, who reports S.H. is physically healthy. S.H.’s mother states he is a

very bright young man who made straight as in high school despite frequent absenteeism. He only has one close

friend and has never been on a date. S.H.’s mother says during high school, S.H. rarely attended school social

functions and spent much of his time in his room working on his computer. On graduation from high school, he

received a full scholarship to a community college but is quite anxious about going and is debating whether he

should turn down the scholarship. When questioned by the psychiatrist, S.H.’s face turns bright red, and his

voice shakes when he speaks. S.H. admits his behavior is not normal but says he is afraid he might “do

something stupid” when he is around people and becomes extremely embarrassed when he has to talk to

anyone. He has wanted to ask a certain girl on a date for 3 years but experienced severe anxiety attacks on the

few occasions he tried to approach her. S.H. is afraid of being turned down and believes no girl would ever

want to date someone like him. The psychiatrist’s diagnosis is social anxiety disorder. What clinical features of

social anxiety disorder are present in S.H.?

S.H. exhibits many characteristic features of the generalized type of social anxiety

disorder. S.H. admits he does not like being around people for fear of

embarrassment, and he generally avoids social situations, which are classic traits of

social anxiety disorder. Symptoms of blushing and shaking voice are also common in

social anxiety disorder, as well as other typical anxiety symptoms such as

palpitations, trembling, sweating, tense muscles, dry throat, hot/cold sensations, and

a sinking feeling in the stomach. S.H. also displays hypersensitivity to rejection and

low self-esteem, and he realizes his behavior and fears are unreasonable. These

symptoms and S.H.’s young age are consistent with a diagnosis of social anxiety

disorder.

S.H.’s case illustrates the substantial disability that can result from this illness.

S.H.’s anxiety disorder has deprived him of normal social development, making

friends, dating, participating in social functions regularly, and pursuit of higher

education. Future impairments throughout S.H.’s life are likely to be significant

unless his anxiety is treated successfully.

TREATMENT SELECTION FOR SOCIAL ANXIETY DISORDER

CASE 83-8, QUESTION 2: The physician decides to initiate sertraline 50 mg every morning for S.H. Is the

prescribed pharmacotherapy appropriate in this case?

Because S.H.’s generalized social anxiety disorder is severely affecting his life,

medication treatment is indicated. SSRIs are first-line therapy for treating social

anxiety disorder, and sertraline is a good choice because it is FDA-approved for this

indication and available as a generic. Although not applicable in this case, sertraline

is also effective for many other psychiatric disorders commonly seen in patients with

social anxiety disorder. The sertraline starting dose of 50 mg/day is appropriate for

S.H., and 50-mg increment dosage increases can be made every 4 weeks according to

response, up to a maximum of 200 mg/day. Signs of response may be seen within 2 to

4 weeks, but 8 to 12 weeks is usually required for optimal results. If available, CBT

may also be combined with pharmacotherapy for S.H.

GOALS AND DURATION OF TREATMENT

CASE 83-8, QUESTION 3: What are the goals of treatment in this case, and how can S.H.’s response to

treatment be objectively assessed? How long should effective therapy be continued?

Three principle domains of treatment outcomes have been defined for social

anxiety disorder: symptoms, functionality, and overall well-being.

54

It is

recommended that all three of these areas are assessed because even if all anxiety

symptoms disappear, treatment is not clinically significant unless functioning also

improves. The clinician-rated Liebowitz Social Anxiety Scale and the patient-rated

Sheehan Disability Scale can be used for measuring improvements in symptom and

functional ability domains, respectively.

54

In S.H.’s case, the desired outcomes of

treatment include reducing fear and avoidance of social situations, enabling him to

comfortably interact socially and attend college, and improving his quality of life.

Several studies have examined relapse rates after double-blind discontinuation of

effective treatment in social anxiety disorder.

132,136,139 Long-term studies have shown

sertraline, paroxetine, escitalopram, fluvoxamine CR, venlafaxine XR, pregabalin,

and clonazepam prevent relapse of social anxiety disorder during continuation

treatment.

20 Therefore, pharmacotherapy should be continued for at least 1 year after

response.

125,132 After that time, a gradual medication discontinuation trial may be

attempted with vigilant monitoring for signs of relapse.

POST-TRAUMATIC STRESS DISORDER AND

ACUTE STRESS DISORDER

Diagnostic Criteria

PTSD and acute stress disorder occur in people who have experienced a severely

distressing traumatic event. These disorders are

p. 1752

p. 1753

characterized by symptoms of intrusive re-experiencing, avoidance features,

autonomic hyperarousal, and negative cognitions and mood symptoms.

1

In addition to

war veterans, PTSD also occurs in persons exposed to events such as natural

disasters, serious accidents, criminal assault, rape, physical or sexual abuse, and

political victimization (refugees, concentration camp survivors, hostages). The

trauma does not have to involve physical injury to the PTSD victim. Witnessing

someone else being injured or killed, being diagnosed with a life-threatening illness,

and experiencing the unexpected death of a loved one are common types of trauma

that may lead to PTSD.

1

Symptoms of PTSD are presented in Table 83-11.

1 According to diagnostic

criteria, the person must have exposure to actual or threatened death, serious injury,

or sexual violence via directly experiencing the event, witnessing the event in person,

learning the event occurred to a close family member or friend, or experiencing

extreme exposure to aversive details of an event.

1 Specifiers indicate whether PTSD

is delayed (after 6 months) onset in relation to the trauma and/or whether it is

associated with dissociative symptoms.

1 Symptoms must persist for at least 1 month

to meet the criteria for PTSD. Acute stress disorder is a separate diagnostic category

in the DSM-5 and refers to cases in which symptoms last less than 1 month (but at

least 3 days).

1

It involves many of the same clinical features as PTSD, and like with

PTSD, symptoms must be severe enough to interfere with functioning.

Epidemiology and Clinical Course

PTSD is associated with a lifetime prevalence in the general population of

approximately 10% and up to 24% among deployed serviceman from Iraq and

Afghanistan.

140 PTSD is twice as common in women, although overall, men are

exposed to trauma more often.

141 Rates of PTSD are expected to rise as the frequency

of traumatic events throughout the world continues to increase. An estimated 80% to

90% of individuals in the United States today will experience at least one event

during their lifetime traumatic enough to lead to PTSD.

141

Most people who are exposed to a traumatic event do not develop PTSD;

approximately 90% of individuals experience a normal acute stress response to

trauma and fully recover.

141 Risk factors for the development of PTSD include

experiencing assaultive violence, more severe and chronic traumas, a history of

depressive or anxiety disorders, lack of social support after the trauma, and

experiencing dissociative or other intense symptoms during or soon after the

trauma.

140–142 Previous exposure to trauma also increases the risk of developing

PTSD after later traumas, and survivors of childhood sexual or physical abuse have

been found to be especially vulnerable.

142,143

Overall, 79% to 88% of PTSD patients also suffer from other disorders in their

lifetime, including major depression, alcohol or other substance abuse, GAD, panic

disorder, and phobic disorders.

140,141,143–145 The risk of suicidality in PTSD is high

and likely influenced by comorbid major depression.

146 Recent studies have also

found associations with PTSD and coronary heart disease, traumatic brain injury, and

sexual dysfunction.

147–149 PTSD causes significant functional disability and has been

associated with school failure, teenage pregnancy, unemployment, marital instability,

legal problems, and impaired performance in the workplace.

150

The course of PTSD is highly variable. Most patients who meet criteria for PTSD

1 month after trauma show spontaneous recovery within 6 to 9 months.

144 PTSD

continues for years in a significant minority, estimated at 10% to 25%, and some

sufferers experience a lifelong course of illness.

Etiology and Pathophysiology

Psychological trauma, especially that which occurs early in life or is chronic in

duration, can cause persistent changes in various aspects of brain functioning and in

neurobiologic responses to stress.

151 Evidence of altered NE, 5-HT, glutamatergic,

GABA system, HPA axis, neuroendocrine, substance P, and opioid system

functioning has been found in PTSD.

152–155 Stress-induced hyperactivity of central

noradrenergic systems is believed to lead to the generalized anxiety and autonomic

hyperarousal associated with PTSD.

153

Neurobiologic consequences of stress and trauma result in both structural and

1.

2.

3.

4.

functional changes in the brain, including reduced hippocampal volume and

excessive activation of the amygdala.

156 Genetic factors may also play a role in

influencing vulnerability to the damaging effects of stress.

157

Table 83-11

Symptoms of Post-traumatic Stress Disorder for Individuals ê6 Years of Age

1

Intrusion (e.g., memories, dreams, dissociative reaction (like flashbacks), intense distress that is experienced

on exposure to stimuli associated with the traumatic event, or physiologic reactions to internal or external

cues that reflect the event)

Avoidance (e.g., avoidance of or efforts to avoid distressing memories, thoughts, or feelings or external

reminders such as places, people, conversations about or related to the event)

Increased arousal including at least two of the following:

Sleep disturbances

Irritability or anger outbursts

Difficulty concentrating

Hypervigilance

Exaggerated startle response

Reckless of self-destructive behavior

Persistent negative alterations in cognition or mood associated with the event including at least two of the

following:

Amnesia surrounding the event

Negative beliefs or expectations about oneself, others, or the world

Distorted cognitions about the cause or consequence of the event where the individual blames themselves

or others

Negative emotionalstate

Diminished interest or participation in activities

Detachment or estrangement

Lack of ability to experience positive emotions

p. 1753

p. 1754

Treatment of Post-traumatic Stress Disorder

Both medications and CBT are useful in treating PTSD. Nonpharmacologic therapies

alone may be appropriate for initial treatment of mild PTSD, but pharmacotherapy,

either alone or in some instances in combination with psychological therapies, may

be recommended for patients with moderate or severe illness.

25,142,143,150,158 When

assessing various treatment options for PTSD, it is important to consider effects on

all four core symptom clusters (re-experiencing or intrusive symptoms, avoidance,

hyperarousal, or negative cognitions and mood symptoms). Not all PTSD treatments

are effective for each domain.

The preferred first-line medications in PTSD are SSRIs or the SNRI, venlafaxine

XR, but various other antidepressants may also be useful. Response to

pharmacotherapy occurs very gradually, taking 8 to 12 weeks or longer. Partial

response at 12 weeks of treatment may be followed by full remission after several

more months of therapy; therefore, an adequate period should be allowed to fully

determine response to a particular medication. Lack of improvement after 4 weeks of

therapy indicates nonresponse, so alternative treatment strategies should be tried in

these cases.

159 Although further research is needed, prevention of PTSD using various

pharmacologic strategies has been evaluated in adults. A recent review highlights

potential utility of hydrocortisone, but additional studies are needed.

160

SELECTIVE SEROTONIN REUPTAKE INHIBITORS AND SEROTONIN

AND NOREPINEPHRINE REUPTAKE INHIBITORS

Sertraline and paroxetine are currently the only FDA-approved SSRIs for PTSD.

Large controlled studies have demonstrated that both agents, as well as venlafaxine,

are effective and superior to placebo.

161 They also have beneficial effects on

depression and general anxiety symptoms and have been associated with

improvements in overall functioning and quality of life.

159,161 Use of fluoxetine also

appears to be effective in treating PTSD in some patients, although study results have

been mixed.

20,25 Citalopram, escitalopram, and fluvoxamine have shown efficacy in

the treatment of PTSD in open trials, but randomized, double-blind, placebocontrolled studies have yielded negative results.

159,162 Finally, one small, naturalistic

study in treatment-resistant men suggests duloxetine may be effective in managing

comorbid depression and PTSD.

163 However, in another small, prospective study in

military veterans suggests additional studies are warranted.

164

OTHER ANTIDEPRESSANTS

Several open studies and case reports suggest nefazodone, mirtazapine, and

bupropion are effective in treating core symptoms of PTSD.

155,165 Although supporting

evidence for these antidepressants is not as strong, they may be considered

appropriate alternatives to SSRIs or venlafaxine in certain patients. The TCAs

amitriptyline and imipramine and the MAOI phenelzine have also been found to be

effective for PTSD in controlled trials, but these agents are generally not

recommended because of their poor tolerability and safety profiles.

143 Because of the

relatively high risk of suicide in PTSD, TCAs can be especially dangerous in this

population.

MISCELLANEOUS AGENTS

Various other medications have been used successfully in limited numbers of PTSD

cases. Anticonvulsants carbamazepine, valproate, topiramate, tiagabine, gabapentin,

oxcarbazepine, vigabatrin, pregabalin, levetiracetam, and lamotrigine have been

studied with inconsistent results, mostly in case series and open-label trials.

20,25,161,165

These agents may be effective in certain patients and can be useful for reducing

irritability, impulsivity, and anger or violent outbursts, particularly in patients with

bipolar disorder.

166 Anticonvulsants may also be effective for intrusive, reexperiencing, and hyperarousal symptoms. Atypical antipsychotic agents

(risperidone, quetiapine, olanzapine) have been used effectively to treat PTSDrelated psychotic symptoms and sleep disturbances, though evidence is limited. One

study failed to find benefit with adjunctive use of risperidone in treatment-resistant

PTSD in military service personnel compared to placebo.

167 However, a recent metaanalysis suggests these agents may help target symptoms of intrusion.

168 The α1

-

adrenergic antagonist, prazosin, may decrease nightmares, increase sleep time, and

reduce other core symptoms in patients with PTSD.

155,169 Higher doses, up to 16

mg/day, may be needed to optimize efficacy.

170 Conflicting evidence exists for the use

of the β-adrenergic antagonist, propranolol, which has been studied in blocking

memory consolidation and therefore may prevent PTSD if administered within hours

of the traumatic event.

171 Larger studies are needed to determine whether this is a

useful preventive option. As previously mentioned, preliminary evidence supports

the use of hydrocortisone for this indication, though additional studies are needed.

160

Benzodiazepines are generally ineffective in treating PTSD, and use of these agents

is not recommended.

172

NONPHARMACOLOGIC TREATMENTS

Various types of psychosocial therapies have been used in the treatment of PTSD,

including anxiety management training to help patients cope with stress.

172 Traumafocused CBT and eye movement desensitization and reprocessing treatment have both

demonstrated effectiveness in PTSD, and either of these treatments are recommended

for all patients with PTSD.

140,158 Cognitive therapies seem to be most effective for

symptoms of demoralization, guilt, and shame, whereas exposure therapies are better

for reducing intrusive thoughts, flashbacks, and avoidance behaviors. Studies are

needed to further investigate the utility of virtual reality exposure therapy and

transcranial magnetic stimulation in PTSD.

173,174 Trials of combined psychosocial

therapies and medication are inconclusive and require further investigation to

determine superior effectiveness compared with either treatment strategy alone.

175

Clinical Presentation of Post-traumatic Stress Disorder

CASE 83-9

QUESTION 1: D.D. is a 42-year-old woman who was attacked and raped in the driveway of her home as

she was getting out of her car 1 month ago. She did not seek medical treatment at the time and waited several

days before reporting the incident to anyone, including her family. She presents to her physician complaining

that she cannot sleep and she is irritable, anxious, and depressed. When asked about any recent stressors in her

life, she finally tells her doctor about the rape. D.D. has no history of psychiatric illness, admits her symptoms

have appeared since the attack, and says she has never had any psychiatric problems until now. She states she

has nightly nightmares and becomes extremely anxious every time she comes home and gets out of her car at

night (which she avoids doing when possible). She is startled when the phone rings or when someone

approaches her unexpectedly, and she literally freezes if she sees a man who bears any physical resemblance

to her attacker. D.D. also states that memories of the rape often flash through her mind for no reason, although

she tries hard not to think about it. The assailant has not been caught, and D.D. feels extremely guilty for not

promptly reporting the crime. Her symptoms are interfering significantly with her ability to work and have put a

strain on her marriage. What clinical features of PTSD does D.D. display?

p. 1754

p. 1755

Individuals with PTSD often present with nonspecific complaints indicative of a

generalized anxiety, depression, or substance use disorder. They may not realize or

want to reveal an association between their symptoms and the trauma experienced.

Careful evaluation by the clinician is required to elicit a pattern suggestive of PTSD.

D.D. displays many target symptoms of PTSD, including re-experiencing/intrusive

symptoms (nightmares, recurrent memories), avoidance of the activity reminding her

of the trauma, symptoms of increased arousal (sleep difficulties, irritability,

exaggerated startle response), and negative alterations in cognition (guilt). In

addition, she is experiencing feelings of depression, distress, marital problems, and

impairment in occupational functioning as a result of her symptoms. The lack of any

previous psychiatric illness combined with the temporal relationship between the

attack and her symptoms supports the presence of PTSD as opposed to another

anxiety or depressive disorder. Since her trauma occurred 1 month ago, her condition

would be classified as acute-onset PTSD.

Treatment Selection and Selective Serotonin Reuptake

Inhibitor Dosing

CASE 83-9, QUESTION 2: What factors are important in the selection of an initial treatment for D.D.?

Because D.D. is exhibiting moderate-to-severe PTSD symptoms, pharmacotherapy

is indicated. Medication treatment should be combined with CBT if it is available,

but nonpharmacologic therapies alone are generally reserved for patients with mild

symptoms. An SSRI is the preferred initial medication treatment for most patients.

161

Sertraline is an appropriate choice of treatment in this case and is FDA-approved for

PTSD. Low initial SSRI doses are recommended in PTSD, so sertraline can be

started at 25 mg/day and gradually increased to the target dosage range of 100 to 150

mg/day, according to response and tolerability.

165 Persistent sleep complaints during

the first month after a traumatic experience may predispose the patient to chronic

PTSD, so management of sleep disturbances is an important component of initial

PTSD treatment.

175

If CBT for insomnia is available, this may be considered.

176