women disappears after menopause, which may necessitate the use of lower
benzodiazepine dosages during the postmenopausal period. Women have slower
glucuronidation metabolic processes than men, resulting in lower clearance of agents
such as temazepam and oxazepam.
Obesity and liver impairment are other physiologic factors relevant to B.G.’s case.
Obesity increases the volume of distribution of benzodiazepines and the extent of
accumulation of long-acting agents. Significant changes in the elimination half-lives
of lorazepam and oxazepam are not observed in obese patients. Liver dysfunction can
reduce benzodiazepine elimination rates and prolong their half-lives, resulting in
recommendations for decreased dosages. The pharmacokinetics of lorazepam,
oxazepam, and temazepam are unaffected by liver disease.
Decreased protein binding of benzodiazepines can occur in patients with renal
insufficiency, which may lead to increased free fractions of highly protein-bound
agents. However, no significant changes in clearance or volume of distribution of
free drug have been noted. Regarding ethnicity, up to 25% of Asians are CYP2C19
poor metabolizers. Decreased clearance of a variety of CYP2C19 substrates,
including diazepam, has been reported in Asian subjects.
In summary, the physiologic factors that can alter benzodiazepine disposition in
B.G. are his age, obesity, male sex, and liver disease. Accumulation of clonazepam
owing to these combined effects probably led to his mental status changes. In
addition to these factors, cimetidine and omeprazole can both increase the exposure
of clonazepam, resulting in decreased clearance and increased side effects.
If continued benzodiazepine therapy is deemed necessary for B.G., lorazepam or
oxazepam would be preferred agents because they are least affected by aging,
obesity, liver disease, or drug interactions. Benzodiazepine dosage equivalencies,
which are based on relative potencies, can be used to determine an equivalent dose
for the selected agent (Table 83-4). However, these equivalencies are inexact, and
dosing conversions should take patient variables and usual dosage ranges into
consideration. For example, B.G. had been taking 1 mg/day of clonazepam, so the
calculated equivalent lorazepam dosage is 3 to 4 mg/day. Because of his age and
recent reaction at this dose, a somewhat lower initial dose of 0.5 to 1 mg BID would
be indicated, accompanied by careful monitoring for adverse effects or withdrawal
symptoms. However, switching to a nonbenzodiazepine agent should be considered
because this may be a better treatment option for B.G.
CASE 83-6, QUESTION 2: Several days after recovery from clonazepam intoxication, B.G. expresses a
to buspirone. How does the clinical profile of buspirone compare with benzodiazepines?
Buspirone lacks CNS depressant effects, sedation, cognitive or psychomotor
impairment, respiratory depression, and muscle relaxant or anticonvulsant effects.
This makes buspirone useful in older patients who may have a variety of chronic
medical conditions. Buspirone is generally well tolerated, and possible side effects
include mild nausea, dizziness, headache, and initial nervousness.
antidepressants, buspirone does not adversely affect sexual functioning and has
actually improved sexual functioning in some patients with GAD.
minimal potential for abuse and is not classified as a controlled substance. It does not
produce physical dependence or withdrawal syndromes on discontinuation, even
It also does not interact with alcohol or other CNS
depressants and is relatively safe in overdose.
Buspirone is a 5-HT1a receptor agonist/antagonist and is as effective as
benzodiazepines such as alprazolam, oxazepam, lorazepam, diazepam, and
clorazepate in the treatment of GAD.
99,100 Like antidepressants, buspirone is more
effective than benzodiazepines in treating the cognitive symptoms of anxiety.
However, the anxiolytic effects of buspirone have a more gradual onset than
benzodiazepines. Initial effects are observed within the first 7 to 10 days, but 3 to 4
weeks may be needed for optimal results. Buspirone must be taken on an ongoing
basis if it is effective, and the drug should not be taken “as needed.”
SWITCHING FROM BENZODIAZEPINE TO BUSPIRONE THERAPY
CASE 83-6, QUESTION 3: How should B.G. be switched from benzodiazepine to buspirone therapy?
Because buspirone has no CNS depressant effects and is not cross-tolerant with
the benzodiazepines, it is not effective in preventing or treating benzodiazepine
withdrawal. Thus, when patients are converted from benzodiazepine to buspirone
therapy, the benzodiazepine must be discontinued gradually. Because it takes several
weeks for full therapeutic effects of buspirone to occur, it can be initiated before the
benzodiazepine taper begins. This may indirectly ease benzodiazepine withdrawal by
providing extra anxiolytic coverage during the benzodiazepine taper period.
Administration with food may significantly increase bioavailability by decreasing
the first-pass effect. Some of the side effects of buspirone, such as nervousness, are
attributed to its active metabolite, 1-pyrimidinylpiperazine (1-PP).
elimination half-life of buspirone is short, approximately 2 to 3 hours, but 1-PP is
The clearance of buspirone is significantly reduced in patients with kidney or liver
disease, but there is little change in side effects or tolerability.
recommended that buspirone dosages be lowered in patients with compromised renal
or hepatic function and that use of the drug be avoided in cases of severe impairment.
Buspirone is metabolized by CYP3A4, and coadministration of CYP3A4
inhibitors, including grapefruit juice, can result in significant increases in buspirone
46 Because of buspirone’s extremely wide margin of safety and tolerability,
even very large increases in its plasma levels may be clinically insignificant.
Buspirone should be avoided in patients taking MAOIs and used cautiously in
combination with high-dose antidepressants because of the risk of serotonin
Some studies suggest patients previously treated with benzodiazepines will not
respond favorably to buspirone.
72,100 However, buspirone may provide benefit in this
population as long as the benzodiazepine is tapered slowly enough to prevent
22 B.G. has been taking diazepam for several months and the drug
needs to be withdrawn gradually during a period of at least several weeks. B.G. can
be started on buspirone at this time. The usual recommended starting dosage of
buspirone is 15 mg/day given in two to three divided doses, but a lower dosage (10
mg/day) is indicated in B.G. because of his liver disease. Twice-daily dosing is
preferred to facilitate compliance and is comparable in efficacy and tolerability to
103 The daily dosage may be increased in 5-mg/day
increments every 3 to 4 days. Optimal anxiolytic doses generally range from 20 to 30
mg/day, with 60 mg/day being the recommended maximum. There are no specific
guidelines for adjusting dosages in patients with liver impairment; therefore, dosage
titrations in B.G. should be made slowly, according to his response and side effects.
The hallmark characteristic of panic disorder is the occurrence of sudden and distinct
panic attacks, which are marked by an overwhelming wave of symptoms and feelings
reaching their peak within 10 minutes. Symptoms are listed in Table 83-9. To meet
diagnostic criteria, at least one of the attacks must be followed by symptoms lasting
at least 1 month, including persistent worry or concern about the consequences of the
attack or significant behavior change related to the attack.
four required symptoms to fulfill diagnostic criteria is termed a “limited symptom
attack.” Three types of panic attacks have been defined with regard to the context in
which they occur: unexpected or uncued panic attacks (the attack is not associated
with a situational trigger); situationally bound panic attacks (the attacks invariably
occur on exposure to a situational trigger); and situationally predisposed panic
attacks (the attacks are more likely to, but do not invariably, occur on exposure to a
Although panic attacks are the hallmark symptom of panic disorder, their
occurrence can also be associated with depressive and other anxiety disorders.
example, situationally predisposed panic attacks may occur in either panic or phobic
disorders. Nocturnal panic attacks, which awaken a person from sleep, are almost
always indicative of panic disorder. Because panic attacks occur unpredictably, they
often lead to generalized anxiety or constant fear of sudden attacks.
Epidemiology and Clinical Course
Although the estimated lifetime prevalence of panic disorder is 6.8%, approximately
10% of persons experience recurrent panic attacks that do not fulfill the diagnostic
criteria for panic disorder and nearly 30% experience a single isolated panic attack
14 The onset of panic disorder often occurs during
stressful periods, usually in the late teens to mid-30s, with rare first onset in the
8,77 Women are affected two to three times more often than men.
Panic disorder, like other anxiety disorders, is accompanied by marked degrees of
psychiatric comorbidity. Common comorbidities include other anxiety disorders,
affective disorders, personality disorders, and alcohol/substance use disorders with
the majority of patients suffering a major depressive episode at some point.
Patients with psychiatric and medical comorbidities have more severe symptoms,
respond more slowly to treatment, have a lower chance of reaching remission, and
have a greater suicide risk (particularly when depression or substance abuse are
present) than those with panic disorder alone.
106 Although most patients experience
episodic periods of remission and relapse, nearly one in five suffer almost
Palpitations, pounding heart, or increased heart rate
Sensations of shortness of breath or smothering
Feeling dizzy, unsteady, lightheaded, or faint
Derealization or depersonalization
Fear of losing control or going crazy
Panic disorder is associated with very high rates of healthcare service
106 The vast majority of patients with panic disorder do not complain of
feeling anxious and report only physical symptoms, such as chest pain, GI problems,
headache, dizziness, and shortness of breath, which contributes to misdiagnosis.
The poor recognition of panic disorder in primary-care settings further increases use
of medical services. Panic disorder is the underlying cause of symptoms in an
estimated 10% to 30% of patients referred to specialty vestibular, respiratory, or
neurology clinics, and up to 60% of those referred for cardiology consultation.
not uncommon for patients to have been in the healthcare system for up to 10 years
before they are correctly diagnosed.
A neurobiologic model for panic disorder has been proposed in which the amygdala
is the central hub of the fear circuit.
5,109 Various projections from the amygdala,
including the hypothalamus and the locus coeruleus, trigger autonomic and
neuroendocrine responses resulting in anxiety and panic attacks. Patients with panic
disorder have a heightened anxiety sensitivity (fear of anxiety-related sensations),
and a variety of substances and situations may activate the anxiety and panic
109 Acute panic attacks are believed to be caused by dysregulated firing in
the LC as described previously (see Neurobiology of Anxiety section), and
hyperresponsiveness of the NE system may be an underlying cause for panic
Other neurobiologic research suggests patients with panic disorder have abnormal
patterns of cerebral glucose metabolism in certain brain areas; abnormalities in
GABA-A receptor, NE, 5-HT, and CCK functioning; decreased GABA-A
benzodiazepine binding sites; abnormal regulation of neuroactive steroids that
modulate GABA-A receptors; hyperactivation of the HPA axis; CCK-B receptor
gene polymorphism; and are hypersensitive to carbon dioxide. These findings seem
to predispose patients to panic attacks and require further study.
Genetic and environmental influences both contribute to a familial pattern where
1,17 The vulnerability is believed to involve
heightened anxiety sensitivity whereby harmless normal physical sensations are
misinterpreted as being dangerous and cause fear.
112 Several studies have shown
distressing childhood events (e.g., separation from parents and abuse) and behavioral
inhibition during childhood (e.g., excessive fear and avoidance of novel stimuli) are
associated with markedly increased risks of developing panic disorder later in
109 No single biologic abnormality can explain panic disorder, and further
research is needed to define the complex interplay of the various pathophysiological,
genetic, and environmental findings in this illness.
Approximately 70% to 90% of patients with panic disorder can experience
substantial relief with currently available treatments, which include both
pharmacologic therapies and CBT.
1,105 Medications and CBT both are beneficial for
reducing panic attacks initially, and their effects on phobic avoidance generally occur
later. First-line medication treatments for panic disorder are SSRIs and venlafaxine
as TCAs are less tolerable and possess more safety and drug–drug interaction
20,25,112,113 Benzodiazepines also are effective but no longer recommended as
first-line treatment given their abuse liability, cognitive and psychomotor
impairments, and lack of efficacy at treating common comorbidities. The
heightened anxiety sensitivity common in panic disorder makes patients especially
vulnerable to initial SSRI and TCA side effects, such as anxiety and agitation. For
this reason, lower-than-usual starting doses of antidepressants are recommended in
SELECTIVE SEROTONIN REUPTAKE INHIBITORS
Paroxetine, sertraline, fluoxetine, and venlafaxine are FDA-approved for treating
panic disorder although other SSRIs (fluvoxamine, citalopram, escitalopram) are
also effective in reducing the frequency of panic attacks, anticipatory anxiety, and
20,25,113 Although low starting dosages are recommended (10
mg/day for paroxetine and citalopram, 25 mg/day for sertraline, 5–10 mg/day for
fluoxetine and escitalopram) to minimize side effects, higher doses relative to
antidepressant doses are usually required for response. The recommended target
dosage range is 20 to 40 mg/day for paroxetine, citalopram, and fluoxetine, 100 to
200 mg/day for sertraline and fluvoxamine, and 10 to 20 mg/day for escitalopram for
112 The initial dose of venlafaxine XR should be 37.5 mg/day with a
recommended therapeutic dose of 150 to 225 mg/day.
Response to SSRIs and other antidepressants in panic disorder occurs gradually,
over the course of several weeks. Reduced frequency of panic attacks usually begins
within 1 to 2 weeks. A trial period of at least 6 weeks should be allowed to fully
assess response, and continued improvements may be seen during a treatment period
The benzodiazepines alprazolam and clonazepam are FDA-approved for treating
panic disorder and are the most extensively studied agents of this class although
lorazepam and diazepam, when used in equivalent doses, also appear effective.
Optimal benzodiazepine dosing is an important issue in treating patients with panic
disorder because these individuals may need higher doses for response than patients
114 This may be related to reduced sensitivity of
benzodiazepine binding sites in panic disorder.
115 An alprazolam dosage range of 4
to 6 mg/day is effective for most panic disorder patients, but others may require up to
10 mg/day for optimal response. The total daily dose usually needs to be taken in
three or four divided doses to minimize breakthrough anxiety or panic attacks before
the next scheduled dose because of fluctuating serum levels given its relatively short
duration of action. The extended-release alprazolam formulation (alprazolam XR)
was developed to address this problem.
It may have a lower abuse liability than
immediate-release alprazolam, but this remains unproven. Patients with panic
disorder are especially sensitive to benzodiazepine withdrawal effects. For these
reasons, using the longer-acting benzodiazepine clonazepam (1–2 mg/day dosed
twice daily) may be preferred over alprazolam.
TRICYCLIC ANTIDEPRESSANTS, MONOAMINE OXIDASE INHIBITORS,
TCAs were the first medications widely used in the treatment of panic disorder.
Imipramine (100–300 mg/day) and clomipramine (50–150 mg/day) are as effective
as alprazolam, but are less well tolerated.
116 Evidence for most other TCAs is
20,25,112,113 Clomipramine appears to be more effective than other TCAs for
panic disorder, perhaps because of its greater serotonergic effects.
lower initial doses to minimize anxiety-like side effect, many patients discontinue
therapy because of poor tolerability.
Among the MAOIs, phenelzine is often heralded as being remarkably effective in
the treatment of panic disorder, but this claim is based on studies conducted before
the publication of the initial diagnostic criteria for panic disorder in 1980.
recent MAOI studies are available to assess phenelzine’s efficacy within the context
of current diagnostic and treatment standards. It is generally an option of last resort
for treatment-refractory cases because of the many clinical disadvantages of MAOIs
relative to other antidepressants (see Chapter 86, Depression).
Preliminary reports suggest mirtazapine may also be beneficial in treating panic
20,112 This agent may be useful in patients who do not respond to SSRI
Other medications that are reportedly effective in treating panic disorder include
anticonvulsants (valproic acid and levetiracetam) and antipsychotics (primarily
risperidone and olanzapine) as either monotherapy or adjunctive therapy used in
20,112 More information is needed before any of these can
be routinely recommended for treating panic disorder.
CBT, including exposure treatment and relaxation training, is also established as
being effective in panic disorder.
105,112 The cognitive theory of panic disorder is
based on the observed heightened anxiety sensitivity in these patients and asserts that
physical anxiety sensations are misinterpreted as being serious or life-threatening.
These fears trigger a cycle of further worsening anxiety symptoms that finally
progress to a panic attack. Reversing the cognitive component of this vicious cycle is
an integral part of CBT and is important in producing lasting therapeutic effects of
112 Breathing retraining and exposure to fear cues are key components of
Some studies have found medications to be superior to CBT in the treatment of
panic disorder, whereas others report opposite results.
with CBT can be useful to increase response/remission rates in those with severe
symptoms or a partial response as well as to improve relapse rates during
pharmacotherapy discontinuation attempts.
Clinical Presentation and Differential Diagnosis of
QUESTION 1: S.K., a 24-year-old female graphic artist, presents to the ED complaining of chest pain,
S.K. exhibits many typical characteristics of panic disorder. As illustrated in this
case, the first panic attack typically occurs without warning while the person is
involved in a normal everyday activity and lasts 10 to 30 minutes. Panic attacks are
extremely terrifying and usually leave the sufferer feeling anxious and convinced
something is medically wrong. As with S.K., it is not uncommon for persons to make
ED visits after or during panic attacks, believing they have had a heart attack or other
serious event. Unfortunately, panic disorder is often not recognized in primary-care
settings, and no medical cause for the symptoms can be identified. Faced with
findings that they are apparently healthy, persons may make repeated ED visits and
consult different doctors and specialists in an attempt to uncover a physical
explanation for their frightening symptoms.
S.K. exhibits the following target symptoms of panic disorder: chest pain,
shortness of breath, dizziness, abdominal distress, and loss of control. Agoraphobia
is present because she avoids leaving her studio because of her fear of having panic
attacks. Other factors consistent with a diagnosis of panic disorder include her young
age, female sex, and lack of abnormal physical findings. This case also illustrates the
association between onset of panic disorder and stressful life events, its common
association with depression, and the frequent lack of recognition of panic disorder in
Because different substances or medical conditions can cause severe anxiety and
panic, it is necessary to rule out these potential causes for panic attacks.
triggers of panic attacks include caffeine, alcohol, nicotine, nonprescription cold
preparations, cannabis, amphetamines, and cocaine (Table 83-2).
marijuana, which can be associated with panic symptoms. Although chronic
moderate-to-severe use of marijuana may complicate the treatment of panic disorder,
it appears infrequent marijuana use does not adversely affect treatment.
does not endorse chronic, severe marijuana abuse, but if she does not adequately
respond to treatment, this might be further explored. Medical illnesses that can cause
panic attacks include thyroid dysfunction, asthma, COPD, mitral valve prolapse, and
122 Panic attacks can also occur with other anxiety disorders.
However, in these cases, the panic attacks usually occur on exposure to a feared
object or situation (in phobic disorders), an object of obsession (in OCD), or a
stimulus associated with a traumatic stressor (in PTSD). S.K. reports her panic
attacks occur unexpectedly, and situationally bound or predisposed attacks are not
evident; therefore, the features are consistent with panic disorder.
Treatment Selection for Panic Disorder, Selective
Serotonin Reuptake Inhibitor Dosing Issues, and
Combination Selective Serotonin Reuptake Inhibitor–
CASE 83-7, QUESTION 2: S.K. is referred to a psychiatrist who decides to initiate treatment with
An SSRI is an appropriate first-line treatment for most panic disorder patients.
patients such as S.K. who have a history of depression, SSRIs may also help prevent
relapse of depression. Patients with severe or distressing symptoms may initially
require concurrent benzodiazepine therapy, which provides quick relief from anxiety
and panic attacks until the therapeutic effects of SSRIs are evident. At that time,
usually after several weeks, the benzodiazepine can be gradually discontinued. An
SSRI–benzodiazepine combination is still the most commonly prescribed initial
treatment, even though guidelines recommend monotherapy unless initial anxiety is
123 Although benzodiazepines are generally avoided in patients with a
history of substance abuse, use of low doses for a limited time may be appropriate
for some patients with disabling symptoms, as long as there is no current substance
20,69,112 Because of the levels of distress and impairment
caused by S.K.’s panic disorder, combined SSRI–benzodiazepine therapy would
have been the preferred initial treatment. Because panic attacks peak quickly and
generally last less than 30 minutes, an as-needed benzodiazepine is not helpful to
prevent panic attacks. As such, scheduled benzodiazepine dosing is preferred over
as-needed dosing schedule during initial therapy.
In choosing among SSRIs for the treatment of panic disorder, paroxetine or
sertraline may be less anxiety provoking in some patients than a more activating SSRI
26 When paroxetine is used, a very low initial dose of 10 mg/day
should be used. In S.K.’s case, the prescribed 20-mg/day starting dose was too high.
Also, scheduled versus as-needed benzodiazepine dosing would have been
preferred. After 2 to 4 weeks, the benzodiazepine can be gradually discontinued
while the SSRI therapy is continued and gradually titrated to the target effective dose.
The potential for drug interactions must also be kept in mind when SSRI–
benzodiazepine combinations are used because certain SSRIs can inhibit
benzodiazepine metabolism, leading to increased benzodiazepine side effects (see
Benzodiazepine Drug Interactions section).
Patient Counseling Information
Patients such as S.K. who are beginning SSRI therapy for the treatment of panic
disorder should be counseled about possible increased anxiety during the first 1 or 2
weeks of treatment, as well as other common SSRI side effects, including nausea,
headache, sexual dysfunction, and either insomnia or sedation. Because these are
dose-related effects, patients should inform their clinician of any problems, and a
dosage reduction may be indicated. These adverse effects (with the possible
exception of sexual dysfunction) usually subside after 1 to 3 weeks of continued
treatment. It is also important to inform patients it may take several weeks before
beneficial effects of antidepressant treatment are seen, and 6 to 12 weeks or longer
may be required for full response. Patients receiving benzodiazepines should be
counseled about their use in providing anxiolytic coverage during the initial weeks of
SSRI therapy, as well as their limited utility as long-term therapy. Other pertinent
counseling information for benzodiazepine treatment should also be included (see
Case 83-2, Question 4). The desired goals of therapy and likely duration of treatment
should also be explained. Providing information about the nature of panic disorder,
including reassurance that panic attacks are not life-threatening, is also important.
Many clinicians recommend patients keep a “panic diary” in which they record
frequency of panic attacks, along with symptoms experienced during attacks.
Clinical Assessment and Goals of Therapy
1 week of escitalopram therapy at the initial dosage of 5 mg/day, S.K. is tolerating the
this case, and how can S.K.’s response to treatment be assessed?
Five domains in panic disorder have been identified in which treatment outcomes
should be assessed: (a) frequency and severity of panic attacks, (b) anticipatory
this case are first to stop S.K.’s panic attacks, then to reduce her anticipatory anxiety,
followed by reversal of phobic avoidance.
54 These outcomes should allow her to
more comfortably leave her studio when required and, secondarily, improve her
overall functioning and quality of life.
Several different instruments have been used to assess outcomes of treatment in
In addition to the panic diary, others include the Fear Questionnaire,
the Panic Appraisal Inventory, and the Panic Disorder Severity Scale. The latter is
currently considered by many experts to be the most useful because it evaluates
outcomes in all five identified target domains of panic disorder.
Course and Duration of Therapy
CASE 83-7, QUESTION 4: After 3 months of escitalopram therapy, S.K. reports she has had no panic
Long-term medication trials in panic disorder support the recommendation that
treatment should continue for at least 6 to 12 months after acute response.
benefits of maintenance pharmacotherapy in preventing relapse are well documented
although the optimal duration of treatment is a subject of continued debate among
panic researchers. Maintenance treatment gives patients time to resume normal
lifestyles and to re-establish daily activities after acute cessation of panic attacks.
In this case, S.K.’s current escitalopram dosage of 20 mg/day is appropriate
because this is within the effective dosage range for panic disorder. Escitalopram
therapy should be continued at the current dosage for 3 to 6 more months. S.K.’s
sexual dysfunction is not likely to decrease with continued treatment; therefore,
specific remedies for SSRI-induced sexual dysfunction may be tried (see Chapter 86,
Depression). After a successful period of full remission, a trial of medication
discontinuation may be attempted to determine whether continued treatment is
necessary. Medication should not be stopped in patients who are experiencing
stressful life events or substantial residual problems in any of the five domains
(frequency and severity of panic attacks, anticipatory anxiety, phobic avoidance
behaviors, overall well-being, and illness-related disability in work, school, and
112 When a medication is discontinued, it should be withdrawn gradually over
several months, regardless of the class. Because of the devastating impact panic
disorder can have, reinstitution of drug treatment is indicated if relapse occurs. Long-
term treatment with antidepressants, and benzodiazepines if necessary, is generally
successful in maintaining treatment benefits without detrimental effects or dosage
SOCIAL ANXIETY DISORDER AND SPECIFIC
Classification and Diagnosis of Phobic Disorders
The DSM-5 includes two primary types of phobic disorders: specific phobia and
social anxiety disorder (formerly social phobia) with symptoms presented in Table
1 These disorders involve excessive or unreasonable fears and lead to
avoidance behavior to minimize anxiety for a duration of at least 6 months. The main
difference between specific phobias and social anxiety disorder is that the former
involves fear and avoidance of specific stimuli and not a general fear of social
Social anxiety disorder manifests as intense irrational fear, anxiety, or avoidance of
scrutiny or evaluation by others in social situations because of concerns about
humiliation or being made to appear ridiculous.
1 A defining feature is that the fears
and anxiety are confined to social situations (e.g., speaking to people, attending
social gatherings, eating or drinking in public, using public restrooms, public
speaking), and patients are usually symptom-free when alone. If the fear is strictly
confined to speaking or performing in public, a performance-only specifier is applied
to the diagnosis. Common symptoms seen in social anxiety disorder include blushing,
muscle twitching, and stuttering, in addition to other typical symptoms of anxiety.
Panic attacks may also occur in either specific phobia or social anxiety disorder on
exposure to the feared object or situation. However, social anxiety disorder is
differentiated from panic disorder in that it involves the fear of scrutiny by others,
rather than the fear of having a panic attack.
Specific phobias are coded by one of five specifiers: animal (e.g., insects, dogs,
spiders), natural environment (e.g., heights, water, storms), blood–injection–injury
(e.g., blood, injury, medical procedures), situational (e.g., flying, bridges, elevators),
1 Significant impairment of functioning or marked distress must be present
for a diagnosis of specific phobia to be warranted. For example, fear of flying might
constitute a diagnosis of specific phobia in a person whose job requires airplane
travel, but it would not impair functioning in someone who never has occasion to fly.
First-line management of specific phobias involves avoidance of the stimuli or
exposure-based psychotherapy, such as CBT or virtual reality exposure. Medications
are not generally considered beneficial, as pharmacotherapy for specific phobia is
largely understudied and psychotherapy is extremely successful. Benzodiazepines
effectively reduce anxiety associated with a phobic trigger, but they may also
interfere with the efficacy of these exposure therapies.
Symptoms of Social Anxiety Disorder (Social Phobia) (Items 1–5) and Specific
or possible scrutiny by others and the person fears humiliation or embarrassment
Experiencing the situation causes an immediate anxiety response
Feared situation is avoided or experienced with intense anxiety or distress
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