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Mod. Prabl. Pharmacopsychiat., vol. 22, pp.

141-173 (Karger, Basel 1987)

Social Phobia
Michael R. Liebowitz
New York State Psychiatric Institute, New York, N.Y., USA

Social phobia, for years the most neglected of the anxiety disorders,
except among behavior therapists, has recently been the subject of in-
creased attention. Research data is now available concerning the preva-
lence, pathophysiology and pharmacotherapy of social phobia. We review
these new findings as well as knowledge regarding classification, severity,
etiology, assessment and behavioral treatments.

Definition

Marks and Gelder [1] initially defined 'social phobia' to include 'fears
of eating, drinking, shaking, blushing, speaking, writing or vomiting in the
presence of other people', the core feature being fear of seeming ridicul-
ous to others. Defined this way, social phobics were found to become
symptomatic and seek treatment earlier, to have a greater male-female
ratio, and to have different anxiety symptoms than agoraphobics [2, 3].
Marks and Gelder's original concept included patients with specific
social fears (fear of speaking, signing a check, or eating in public) and
those with more generalized forms of social anxiety (fears of initiating con-
versations or dating). This 'broad' definition has been challenged in sev-
eral ways.
Some believe that patients with generalized social anxiety should be
classified as avoidant personality disorder [4], and restrict social phobia to
patients with discrete or specific forms of performance or social anxiety.
However, no empirical basis exists for this distinction. In the absence of
data, arbitrarily viewing socially fearful patients as personality disordered
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carries the risk that pharmacological interventions will not even be tried.
This is due to the frequent assumption that personality disorders are
necessarily medication resistant and will only respond to proper
psychotherapy.
The original DSM-III description of social phobia suggests a broad
definition. However, the examples given in the DSM-III description are
all limited to specific social fears, e.g. anxiety about speaking or perform-
ing in public, using public lavatories, eating in public, and writing in the
presence of others. Moreover, DSM-III asserts that social phobics gener-
ally have only one fear, implying that patients with multiple fears or more
generalized social anxiety are either rare or should be included in some
other diagnostic category. Also, without empirical justification, DSM-III
excludes patients from the social phobia category whose social anxiety
symptoms are due to avoidant personality disorder, although the grounds
for this differential diagnosis are not clear.
Also problematic is how to classify patients who develop spontaneous
panic attacks leading to panic disorder or agoraphobia and then begin to
avoid certain performance or social situations for fear of humiliation if
they have a panic. By DSM-III criteria, such social performance avoidance
is secondary to panic disorder (or agoraphobia), and thus not social
phobia. Yet such patients ('secondary' social phobics as opposed to 'prim-
ary' social phobics with no history of spontaneous panic attacks) are moti-
vated by fear of embarrassment or humiliation were they to have a panic
attack in front of others, to avoid giving speeches, giving parties, etc.
An important difference is that primary social phobics fear scrutiny or
evaluation by others, and their anxiety is confined to such situations or an-
ticipation of such situations. Patients with panic disorder or agoraphobia
with panic attacks, on the other hand, also have panic attacks in a variety
of nonsocial situations (subways, supermarkets, tunnels, bridges), and
tend to fear or avoid any situation where easy or unobtrusive exit is dif-
ficult.
Patients with panic disorder are also comforted by the presence of
familiar figures when experiencing anxiety, while primary social phobics
feel more comfortable when alone. Developmental, biological, treatment,
family, and follow-up studies are needed to determine the similarities and
differences between primary and secondary social phobics.
DSM-III R more clearly differentiates social phobia from social or
performance anxiety following panic attacks. The fact that many social
phobics have numerous fears and generalized social anxiety rather than a
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Social Phobia 143

single fear or simply discrete performance anxiety is also noted. The over-
lap of social phobia and avoidant personality disorder is also acknow-
ledged.

Distinction from Other Disorders

Demographic and clinical data support a distinction between social


phobia and agoraphobia. Two studies have found demographic differences
between the two phobic subtypes.
In Marks' [2] series, the social phobics were 50% male, had an average
age of onset of 19 years, and sought treatment at a mean age of 27 years;
agoraphobics were 25% male, had a mean age of onset of 24 years, and
sought treatment at an average of 32 years. While these differences were
not statistically significant, Aimes et al. [3] reported similar differences
that were significant. Of 87 social phobics, 60% were male vs. 14% male
among 57 agoraphobics. There were also significant differences in referral
age (30.7 years for social phobics vs. 37.2 years for agoraphobics). The
high proportion of males makes social phobia unique among the phobias.
Somatic anxiety symptoms reported by social phobics may also show
differences from those of agoraphobics. While further investigations are
needed, in one series, the social phobics reported more blushing and mus-
cle twitching, and less limb weakness, breathing difficulty, dizziness or
faintness, actual fainting, and buzzing or ringing in the ears than did
agoraphobics [3]. These symptom differences suggest that panic attacks
and social phobic anxiety are pathophysiologically distinct. Social phobics
were also found to have lower extraversion scores on the Eysenck Person-
ality Inventory than agoraphobics, whose scores were similar to normal
controls [3].
Findings from biological challenge and treatment studies can also
clarify the relationship of social phobia to panic disorder and agoraphobia.
Patients with panic disorder and agoraphobia with panic attacks show high
rates of panic during sodium lactate infusion [5, 6].
Our preliminary finding, reported in detail elsewhere [7], is that social
phobics show a much lower rate of panic to sodium lactate infusion than
agoraphobics. As part of a larger study, nine patients meeting DSM-III
criteria for agoraphobia with panic attacks, and 15 patients meeting DSM-
III criteria for social phobia, were challenged with 0.5 M racemic sodium
lactate (10 ml/kg of body weight) administered intravenously over 20 min.
As judged by a psychiatric evaluator 'blind' to patient diagnosis, 4 (44%)
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of 9 agoraphobics panicked during the lactate challenge, in contrast to 1


(7%) of 15 social phobics (p~O.03).
Patients with spontaneous panic attacks are highly responsive to the
tricyclic imipramine [8, 9], and the monoamine oxidase inhibitor (MAOI)
phenelzine sulfate [10]. However, the responsiveness of social phobics to
these medications is as yet unclear. As discussed in the 'treatment' section,
preliminary evidence suggests that social phobics may be as responsive to
MAOIs as patients with panic disorder or agoraphobia, but seem to differ
in that they may be more responsive to B-adrenergic blockers. Family and
follow-up studies of social phobics, now lacking, may also clarify its rela-
tion to agoraphobia.
Some evidence supports the distinction between social phobia and the
simple phobias, which consist of specific animal (birds, cats, insects) and
situational (heights, darkness, thunderstorms) phobias. Marks and Gelder
[1] found social phobics to differ in age of onset from simple phobics, while
in a later study, Marks [2] found social phobics to have a later age of onset,
higher overt anxiety level, and higher Maudsley Neuroticism scores than
animal phobics. Lader et al. [11] also found social phobics to have more
spontaneous fluctuations in galvanic skin response than animal phobics,
although in this regard, the social phobics did not differ from
agoraphobics. Weerts and Lang [12] also found students fearful of spiders
to react with greater affect and greater changes in heart rate to fear relev-
ant scenes than students fearful of public speaking.
We lack the data to definitively compare drug responsiveness of social
and simple phobics. Simple phobics have been found unresponsive to
tricyclics [8], and only weakly, if at all, responsive to B-adrenergic block-
ers [13, 14]. One study found 160 mg oxprenolol effective in suppressing
the increase in heart rate during prolonged exposure and making it more
comfortable. Fear and avoidance scores were lower at the end of exposure
in the placebo control group, however, suggesting that the medication re-
tarded de conditioning [13]. In a second study of spider and snake phobics,
tolamalol, a cardioselective, beta-blocker, abolished exposure induced
tachycardia, but had no beneficial sUbjective or behavioral effects [14].
Controlled studies of these agents in social phobia, as well as further stud-
ies of simple phobics, remain to be done. Family history and follow-up
studies may also help to clarify the degree of distinctness between social
phobics and simple phobics.
Social phobics appear distinct from schizoid patients. Although both
avoid social interactions, by definition, the social pbobics desire social
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contact but are blocked by anxiety, while schizoid patients apparently lack
interest in social interaction. Schizophrenics may appear socially phobic,
but their social anxieties seem secondary to the primary disorder. How-
ever, the commonalities of social anxiety in schizophrenic and nonschizo-
phrenic populations remain to be assessed.

Magnitude of the Problem

While epidemiological studies have indicated that phobic disorders


may affect as much as 7% of the general population [15], the prevalence
of social phobia is only now being investigated. Preliminary data from a
multi site psychiatric epidemiological investigation reveal that the 6-month
prevalence of social phobia in two urban populations ranged from 0.9 to
1.7% for men and 1.5 to 2.6 % for women [16]. However, these figures are
based on responses to screening questionnaires, where patients whose so-
cial anxiety was part of another disorder (such as agoraphobia with panic
attacks) would also be counted as socially phobic. Therefore, the preva-
lence of phobic syndromes meeting DSM-III criteria for social phobia
would be lower, and the sex ratio may change. Other data available for so-
cial phobia, such as a 1971 questionnaire survey by Bryant and Trower
[17], estimated that approximately 3-10% of first-year students at a British
college manifested typical social phobic symptoms.
Looking at clinical samples, Marks [2] found 8% of a Maudsley Hos-
pital phobic population to have social phobia, while 60% were
agoraphobic. Other investigators, however, have found a higher ratio of
social phobics to agoraphobics among treatment applicants, once the in-
vestigator's interest in social phobia became known [3]. Among outpa-
tients applying for treatment to one American anxiety and phobia center,
8 (13.3%) of 60 were found to be social phobics, which equaled the pro-
portion with panic disorder and was exceeded only by the 38.3% with
agoraphobia [18].
In our Anxiety Disorders Clinic, social phobics represent the third
most common anxiety disorder (after panic disorder and agoraphobia).
Moreover, some patients with panic disorder or agoraphobia have a his-
tory of social phobia that predates the onset and persists after successful
treatment of their panic attacks.
In terms of morbidity, social phobia seems to begin early (characteris-
tically between ages 15 and 20 years) and to follow a chronic, unremitting
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course [1-3]. Interestingly many patients show no particular evidence of


shyness prior to adolescence.
The symptom pattern appears rather standard; in one series of 11 pa-
tients meeting DSM-III social phobia criteria recently studied by us, all
complained of tachycardia, pounding heart, trembling and sweating
when in performance or a social situation. The attendant disability, in
terms of vocational and social impairment, is often significant. Two of the
11 patients were unable to work, 2 dropped out of school, 4 had abused al-
cohol, 1 had abused tranquilizers, 6 were blocked from work advance-
ment, and 5 avoided almost all social interaction outside their immediate
family.
Significant depressive symptoms are reported to be quite common in
social phobics, and were found in half of the patients in one large sample
[3]. In a similar series, one-third of the patients were found to have either
a past or present history of depression [19]. Among our patients, 5 of 11
had either past or present secondary major depression. Aimes et al. [3]
also found that 14% of their social phobics had a history of suicide at-
tempts, which exceeded the 2% rate among agoraphobics.
Social phobic symptoms are also frequently found among alcoholics,
usually predating the drinking problem [20, 21]. In one sample of 102 alco-
holics admitted to an alcoholism treatment unit, 25% of the men and 17%
of the women were social phobics, meaning that they experienced dis-
abling anxiety in or could not face social situations when not under the in-
fluence of medication or alcohol [20]. A further 35% of the men and 28%
of the women were rated as 'borderline' social phobics because they ex-
perienced social anxiety that was subjectively distressing but not disabling
or accompanied by marked avoidance. Surprised by these findings, Smail
et al. [21] attempted to replicate them, and found that of 60 abstinent alco-
holics surveyed, 39% suffered from social phobia during their last typical
drinking period. Sixty percent to 70% of the social phobic alcoholics re-
ported alcohol helpful in coping with social anxiety. In another study, 20%
of the social phobics were found to consume excessive amounts of alcohol,
significantly more than the 7% of agoraphobics who did so [3].

Pathophysiology and Etiology

It is unclear if normal and pathological social (or performance) anxi-


ety lie on a continuum or are categorically distinct. A certain degree of so-
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cial or performance anxiety is ubiquitous and may have evolutionary adap-


tive advantage by motivating preparation and rehearsal for important or
novel interpersonal events. Such anxiety in normals, however, lessens with
repeated exposure and, indeed, usually attenuates over the course of any
given performance or social encounter [22]. Also social anxiety in normals
is realistically proportional to the real danger of the situation, e.g. a job in-
terview or marriage proposal.
As with simple phobics, the anxiety of the social phobic is out of
all proportion to the reality of the threat. Also, social phobics often re-
port their symptoms to be refractory to self-administered rehearsal or
exposure. (Few have participated in systematic exposure or desensi-
tization programs.) Moreover, their anxiety does not attenuate during
the course of a single social event or performance. Rather, they often
report that their symptoms augment, as initial somatic discomfort be-
comes a further distraction and embarrassment to the already nervous
individual, leading to further symptoms, which gives rise to more distrac-
tion, etc. Systematic studies are needed to determine if and, if so, why so-
cial phobics lack the ability to habituate in social or performance situa-
tions.
The symptoms social phobics experience when feeling under evalua-
tion or scrutiny virtually always include tachycardia, sweating and trem-
bling, all suggesting heightened autonomic arousal. Since normal individ-
uals have brief twofold to threefold increases in plasma epinephrine levels
during stressful public speaking [22], it is tempting to speculate that social
phobics either experience greater or more sustained increases or are more
sensitive to normal stress-mediated catecholamine elevations. These two
possibilities can be examined experimentally by in vivo biochemical
monitoring of social phobics in their feared situations and challenges with
epinephrine infusions.

Epinephrine Challenge Study


Eleven social phobic patients were given intravenous infusions suffi-
cient to raise plasma epinephrine to the 850-1,000 pg/ml range from an 85-
125 pg/ml range within 30 min.
Epinephrine was not potent in provoking anxiety attacks in these
patients. Only 3 patients reported significant anxiety, while only one ex-
perienced the full symptomatology of naturally occurring social anxiety,
and even this was for a briefer than usual duration [Papp et aI., unpubl.
data].
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Liebowitz 148

In vivo Challenge Study


Ten social phobic patients and 7 normal controls underwent a public
speaking simulation while facing a video camera and several staff members.
Heart rate and blood chemistry were directly monitored. Patients started
and remained more anxious than normal controls, but did not reach anx-
iety levels during the procedure equal to their naturally occurring
episodes. Both patients and controls had similar sitting baseline plasma
epinephrine values, and both showed a 20 pg/ml rise when rising from sit-
ting to standing. Patients then showed an additional 20 pg/ml rise at the
anticipatory point which persisted throughout the lO-min speech. Con-
trols, on the other hand, remained at their standing 'baseline' epinephrine
level throughout the procedure. Mean change in patients epinephrine
levels from standing to peak level during the speech was approximately
80%, and significantly exceeded mean change in controls which was ap-
proximately 25% (p:::::0.05, 2-tailed) [Levin et aI., unpubi. data]. In addi-
tion, one limitation of this study was that not all the social phobics were
particularly fearful of public speaking. As a larger series is studied, data
from those with specific public speaking fears can be analyzed separately.
These two experiments suggest the following:
(1) Increasing plasma epinephrine levels is not sufficient to produce
the full scope of social anxiety symptoms in social phobics. This suggests
that social phobia cannot be accounted for by a simple model of hyper-
sensitivity to normal stress-related epinephrine elevation. However, eleva-
tion in the laboratory situations occurred less rapidly than might occur in
real life. Therefore, more rapid epinephrine elevations in laboratory set-
tings need to be studied.
(2) Social phobics seem to produce greater adrenalin levels than nor-
mals during in vivo performance situations. If sustained with larger and
more homogeneous samples and other performance or social procedures,
this finding would support the hypothesis that social phobic symptomatol-
ogy is due in part to the excessive release of adrenalin.
As discussed in the section on 'Treatment', most studies in normal
volunteer samples (analogue studies) [22-23] suggest that B-adrenergic
blockers are quite helpful in reducing performance anxiety, which is con-
sonant with peripheral catecholamine mediation of social phobic symp-
toms, although other mechanisms of action are possible. If this holds for
clinical populations, social phobic anxiety may differ from panic attacks,
which do not appear to be prevented by B-adrenergic blockers [34-38],
and appear mediated by central sympathetic mechanisms 139].
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Social Phobia 149

To date, no family studies of social phobia have been conducted, so


no genetic hypotheses can be tested. Social anxiety may, however, have an
inheritable component. Torgersen [40] compared social fears among 95
monozygotic and dizygotic twin pairs. The monozygotic twins were sig-
nificantly more concordant for such social phobic features as discomfort
when eating with strangers or when being watched working, writing, or
trembling, suggesting a genetic contribution to social anxiety.
Sheehan [41] has postulated that social phobias are one aspect of an
'endogenous anxiety disease'. This is based on the observation that follow-
ing the onset of panic attacks, many individuals begin to avoid perfor-
mance or social situations, then go on to develop more widespread phobic
avoidance (agoraphobia). However, this conflates primary and secondary
social phobia. Also, many individuals with social phobia never develop
panic attacks or nonsocial phobias, arguing against a common diathesis for
social phobia and panic disorder or agoraphobia. There is also no evidence
that social phobia responds to tricyclic antidepressants, which would also
distinguish it from panic disorder and agoraphobia with panic attacks.
Among the postulated acquired causes of social phobia are social
skills deficits, traumatic early social or performance experiences, and
faulty cognitions [42, 43]. Ost and Hugdahl [44] mailed a questionnaire
concerning the origin of the phobias to 34 social phobics attending an out-
patient clinic. Of the 31 who replied, 18 (58.1%) cited conditioning, 4
(12.9%) cited vicarious experiences, 1 (3.0%) cited instruction or informa-
tion from others and 8 (26.09%) said they could not recall the origins of
their phobia. Aside from the issue of accuracy of retrospective self-evalu-
ation, the conditioning attribution needs further refinement. An indi-
vidual may have normal social skills and encounter an unusually unfavor-
able social or performance situation, or deficient skills that render an
otherwise average situation traumatic.
Leary [45] attempts to integrate the conditioning, social skills deficits
are cognitive hypotheses of social anxiety by noting that current explana-
tions of classical conditioning emphasize the role of cognitive processes,
and that people feel socially anxious when they believe they lack, not
when they actually lack, important social skills. As noted by Nichols [46],
many social phobics also appear hypersensitive to rejection or criticism,
suggesting an overlap with atypical depression or hysteroid dysphoria,
where extreme rejection sensitivity is a cardinal feature [47, 48].
The traditional psychoanalytic view that phobias represent the trans-
formation of internal anxiety over an unconscious drive, e.g. exhibition-
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Liebowitz 150

ism, into external fear through displacement, and that the specific content
of a phobia has symbolic meaning [49], is also theoretically applicable to
social phobia. This has not as yet, however, been subject to systematic
controlled investigation.
Nichols [46] has catalogued a variety of other psychological and soma-
tic traits observed in a social phobic sample. These include low self-evalu-
ation; an unrealistic tendency to experience others as critical or disapprov-
ing; rigid concepts of appropriate social behavior; negative fantasy-pro-
ducing anticipatory anxiety; an increased awareness and fear of scrutiny by
others; a fear of social situations from which it is difficult to leave unobtru-
sively; an exaggerated awareness of minimal somatic symptoms, such as
blushing or feeling faint; a tendency to overreact with greater anxiety to
the somatic symptoms of anxiety; and an exaggerated fear of others notic-
ing that one is anxious. It is unclear, however, which among these or other
factors are causal, which are consequences of, and which are not even
specifically related to social phobia.
Several controlled studies have also compared how adult social
phobics, agoraphobics, simple phobics, and normal controls retrospec-
tively rate their parents' child-rearing practices and attitudes. In one study
social phobics scored both parents simultaneously as having been less car-
ing and more overprotective than did normal controls, while agoraphobics
differed from controls only in reporting less maternal care [50]. In a sec-
ond study social phobics and height phobics, as compared to normal con-
trols, again perceived their parents as not only lacking in emotional
warmth, but also rejecting and overprotective. In this study, agoraphobics
reported both parents as having lacked warmth but only their mothers as
being rejecting [51]. However, no contrasts were carried out among the
phobic groups, so the specificity of these findings for social phobics is un-
certain. These studies also suffer from the deficiencies inherent in retro-
spective, subjective assessment.

Assessment

Various investigators have employed subjective (rater and self-assess-


ments), biological, and performance measures to assess social phobics.
Several structured interview schedules designed to facilitate diagnostic
evaluation of anxiety patients are currently under development or in test-
ing. Using one called the Anxiety Disorders Interview Schedule, DiNardo
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Social Phobia 151

et al. [18] found that pairs of trained clinicians achieved a test-retest relia-
bility K of 0.77 for diagnosing social phobia, which is considered quite
satisfactory.
Several self-rating scales with demonstrated reliability appear rele-
vant to social phobics. These include the Willoughby Personality
Schedule, a 25-item scale containing 14 items pertinent to social phobia
[52]; the Fear Questionnaire developed by Marks and Mathews [53],
which contains a social phobia subscale; the Social Avoidance and Distress
Scale, a 28-item true-false inventory; and the Fear of Negative Evaluation
Scale, a 30-item true-false inventory, both developed by Watson and
Friend [54]; and the interpersonal sensitivity subscale of the 90-item Hop-
kins Symptom Check List (SCL) [55].
There are few studies, however, reporting use of these scales with so-
cial phobics diagnosed according to DSM-III criteria. Patients meeting
DSM-III criteria for social phobia have been found to have higher Wil-
loughby Personality Schedule scores than patients with agoraphobia or
simple phobia, suggesting utility for this scale [56]. The Social Avoidance
and Distress and Fear of Negative Evaluation scales have been used to
study socially inadequate psychiatric patients [57] and socially anxious
community residents [58]. At present, no one scale has demonstrated
superiority, and investigators should use a battery of several self-rating
scales.
No existing scale meets the need for an interviewer rated instrument
that assesses the full range of performance and social difficulties that social
phobics report. We, therefore, created a 24-item scale (table I) that has
the following properties: (1) contains a broad range of items social phobics
have difficulty with; (2) has separate subscales for performance and social
anxiety features; (3) has separate ratings for fear or anxiety and avoi-
dance, and (4) in all patients 4 sub ratings are given - performance fear or
anxiety, performance avoidance, social fear or anxiety, social avoidance.
While this instrument appears sensitive to treatment-induced changes
in a social phobic population, it has not yet been systematically tested in
other diagnostic groups.
Biological monitoring of social phobics in resting and performance
situations has mainly involved measurement of heart rate, respiration, and
skin conductance [12, 59, 60]. Lande [59] found that heart rate, respiration
rate, and subjective anxiety were highly correlated during prolonged im-
aginal flooding of two social phobics. Johansson and Ost [60] monitored
heart rate in 34 social phobics who participated in a short conversation
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Table I. Liebowitz Social Phobia Scale

Fear or anxiety Avoidance


O=none O=never (0%)
l=mild 1= occasionally (10%)
2=moderate 2=often (33--67%)
3=severe 3=usually (67-100%)

1 Telephone in public (P)


2 Participating in small groups (P)
3 Eating in public places (P)
4 Drinking with others in public places (P)
5 Talking to people in authority (S)
6 Acting, performing or giving a talk
in front of an audience (P)
7 Going to a party (S)
8 Working while being observed (P)
9 Writing while being observed (P)
10 Calling someone you don't know very well (S)
11 Talking with people you don't
know very well (S)
12 Meeting strangers (S)
13 Urinating in a public bathroom (P)
14 Entering a room when others are
already seated (P)
15 Being the center of attention (S)
16 Speaking up at a meeting (P)
17 Taking a test (P)
18 Expressing a disagreement or disapproval
to people you don't know very well (S)
19 Looking at people you don't know very well
in the eyes (S)
20 Giving a report to a group (P)
21 Trying to pick up someone (P)
22 Returning goods to a store (S)
23 Giving a party (S)
24 Resisting a high pressure salesperson (S)
Total score
Performance (P) anxiety subscore
Social (S) anxiety subscore
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Social Phobia 153

with a person they did not know of the opposite sex, and found significant
increases in heart rate that were highly correlated with self-perceived
physiological arousal.
In contrast, a comparison group of 36 claustrophobics who were
placed in a small room experienced less heart rate increase and negative
correlations between perceived and actual physiological arousal. In inter-
preting the differences between the two phobic groups, it is important to
note fundamental differences in the test situations. Premature exit from
the anxiety-evoking situation was easy for the claustrophobics but not per-
mitted for the social phobics. This may have prevented the claustrophobics
from experiencing the same degree of physiological arousal. Less accurate
self-perception of arousal in the claustrophobics could be due to both the
less intense arousal experienced, and also a blurring of the distinction be-
tween actual arousal and anticipated arousal in patients who left the en-
closed room prematurely.
Measures not yet studied in social phobics might also include cardiac
rhythm (to detect possible arrhythmias in subjects under stress) and in
vivo biochemical monitoring of catecholamine levels, free fatty acid levels,
cortisol levels, etc. A major limitation of biological-dependent measures
for pharmacological studies is that most classes of psychotropic drugs in-
fluence biochemical and physiological factors regardless of therapeutic ef-
fects. Biological monitoring as an index of change is thus most suitable for
nonsomatic or placebo treatment studies.
Performance evaluations can involve observations by professional or
patient peer raters before and after treatment [61, 62], observation during
role rehearsal in simulated situations in the clinic [61], or evaluation of pa-
tient responses in staged situations where the patient is unaware of the
staging, such as when research assistants call patients and pretend to be in-
trusive high-pressure salespeople [61]. All require further study in regard
to utility. Interestingly, social phobics rate themselves more anxious in
performance situations than do peer observers [63], suggesting that exclu-
sive reliance on one or the other source may be misleading.

Treatment

Two types of treatment for social phobia have been subject to at least
some controlled evaluation. These are pharmacotherapy and behavioral
therapy.
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Liebowitz 154

Pharmacological Treatment of Social Phobia


Social phobia has not been regarded by pharmacologists as a discrete
syndrome in need of independent study. Instead, it has been viewed as a
more severe form of a normal human trait (social anxiety) whose treat-
ment could be elucidated by analogue rather than clinical studies [23-33];
a manifestation of one or more personality disorders that are a priori un-
responsive to drug treatment [4]; or as so similar to agoraphobia [64-70] or
simple phobia [9] that the groups could be merged rather than studied in-
dependently.
The unfortunate result is that, with the exception of several small
studies [71-73], no data on the drug responsiveness of a pure social phobic
sample have been reported. Analogue and clinical studies in mixed diag-
nostic groups, however, are suggestive of possible MAOI and B-adrener-
gic blocker efficacy.

MAOIs
Several types of data suggest possible MAOI efficacy for social
phobics. Four controlled studies found positive phenelzine effects in pa-
tient samples that consisted of both agoraphobics and social phobics (table
II) [64-67]. However, none reported response among the social phobics
separately from the sample as a whole. Since agoraphobic patients benefit
from MAOIs [10, 74], it is impossible to be sure that the social phobics be-
nefited from MAOI therapy. Also limiting the usefulness of those studies,
were lack of specified diagnostic criteria, low dosages (45 mg/day or less of
phenelzine sulfate in two), small sample sizes, and no specification as to
whether patients also suffered spontaneous panic attacks or associated de-
pressive features.
Nevertheless, all four studies did find some superiority of phenelzine
over placebo. The earlier Solyom et al. [65] study found a significant
phenelzine effect on social maladjustment. In the Mountjoy et al. [66]
study, phenelzine was significantly better than placebo in lowering social
phobia scale scores for all phobic patients; also, fear of telephoning in pub-
lic was the only measure to show significant correlation with overall im-
provement with phenelzine among patients as a whole.

Phenelzine Study. As a preliminary to embarking on controlled trials


of MAOIs in social phobia, we conducted an open pilot study of phenel-
zine in 11 patients meeting DSM-III for social phobia.
Subjects were recruited from among outpatients presenting for treat-
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Social Phobia 155

Table II. Controlled trials of MAGIs in social phobia

Source Sample Design Daily Duration Final Limitation


completers dosage outcome

Tyrer et al. agoraphobia phenelzme up to 8 weeks phenelzine supenor outcome of


[64] and social sulfate vs. 90 mg/day to placebo on agoraphobics
phobia placebo secondary phobias and SOCial
(n=32) (patient-rated) and phoblcs not
over all outcome reported
(psychiatrist rated) separately;
unclear If
patlents had
pamc attacks
SOlrm et al. agoraphobia, floodmg vs. up to 3 months floodmg produced only phenelzme
[65 social phenelzme 45 mg/day greater decrease on vs. placebo
phobia, plus bnef Wolpe Lang Fear contrast assessed
specific psychother- Survey than other blindly; results
phobia apy vs treatments; slgmfi- not presented
(n=30) placebo plus cant phenelzine- separately for
bnef placebo difference in different types of
psychother- reductIOn of phobia, phobias;
apy neurotic symptoms presence of panic
and SOCial maladJust- attacks at
ment, 6 of 6 patlents basehne not
stoppmg phenelzme speCIfIed or rated
therapy relapsed by
2-year follow-up
Mount/oyet anxiety phenelzine phenelzine 4 weeks phenelzme plus heterogeneous
al. [66 neurosis plus to 75 mg/day; diazepam superior sample; duratIOn
(n=36) diazepam vs. diazepam on SOCial phobia short; small n's
agoraphobia placebo plus 5mg scale for all phobiC for different
or social diazepam 3 times/day patlents; placebo treatment groups
phobia plus diazepam Within each
(n=22) superior on Hamilton diagnosIs; pamc
depressive, Anxiety Scale in attacks not rated
neurosis (not anxiety neurotics at baselIne or
discussed completIOn
herem)
SOlrm et al. agoraphobia 2x2 phenel- up to 6 weeks phenelzme greater data not
[67 or social zine vs. 45 mg/day than placebo on reported
phobia placebo; anxiety reduction separately for
(n=40) exposure vs. during exposure; two types of
no exposure exposure supenor phobias; low
to nonexposure on phenelzme dose;
several measures; lack of control
no sigmficant for exposure;
differences between panic attacks not
exposure and speCified or rated
phenelzme

ment at an anxiety disorders research clinic. Subjects had to be aged 18-


60, speak English fluently, have no serious medical problems, not be in a
current major depression, meet DSM-III criteria for social phobia, and
not have been previously treated with phenelzine 45 mg/day or its equiv-
alent of another MAOI. Patients 1-5 and 11 (see table III) were treated
with phenelzine after failing to fully respond to trials of the cardioselective
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Liebowitz 156

beta adrenergic blocker atenolol and/or the nonselective beta-blocker


propranolol. The sixth patient was initially misdiagnosed as an agora-
phobic, showed a poor response to imipramine, was reevaluated and dis-
covered to be a social phobic, and then treated with phenelzine. The
seventh, eighth and ninth patients were given phenelzine as their first
treatment at our clinic. Patient 10 was treated openly with phenelzine after
failing to respond to placebo in a double blind study. All social phobics
openly treated by us with MAOIs to date are included in this series.
All patients were instructed in what foods, beverages and medications
to avoid. Phenelzine was administered in an open clinical fashion starting
at 30 mg/day for the first week and then going up by 15 mg/day per week
to a possible maximum of 90 mg/day. Patients were seen weekly by a study
psychiatrist but not offered any kind of psychotherapeutic intervention
other than the general instruction to try as best they could to enter feared
situations.
Demographic and clinical findings are shown in table III. Patients
ranged in age from 19 to 44 years. Eight of eleven were male, in keeping
with the previously reported findings that social phobics tend to be more
male than female [2, 3]. Duration of illness ranged from 3 to 20 years of
continuous symptoms. Patients 1, 7, 8 and 9 had histories of major depres-
sion; patients 1 and 4 histories of mild obsessive-compulsive symptoms;
patients 3 and 7 histories of drug abuse; patient 7 current mild alcohol
abuse; and patient 9 a history of post-traumatic stress disorder that began
many years after the onset of social phobia. None of the 11 patients met
Research Diagnostic Criteria (RDC) for current major, minor or intermit-
tent depression. Patient 3 met DSM-III for dysthymia and patients 2 and
8 had brief (several days to a week) mild depressive episodes in the month
prior to the study.
Baseline symptoms rather uniformly included episodes of tachycar-
dia, palpitations, sweating and trembling. Less frequently, patients experi-
enced shortness of breath, blushing, dizziness, lightheadedness or
diarrhea. All episodes were provoked by and confined to performance or
social situations.
The patients did not suffer spontaneous panic attacks, and only 2 (3
and 11) had generalized anxiety disorder as well. Social limitations varied
from excessive discomfort at parties or when meeting strangers (patient 2),
to almost complete social isolation (patients 1 and 6). Similarly, vocational
restrictions varied from a limitation on job choice and advancement (pa-
tient 2), to complete inability to work or attend school (patient 1).
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Table Ill. MAOI treatment of social phobics
C/J
0
Pa- Background Baseline Baseline PrevIous Phenelzine D.
~
tlent data symptoms disability therapy response
"'::I
::r
0
19-year-old male with 4-year rapid heart beat, hand avoidance of social encoun- moderate response to marked response In 4 weeks - cr'
2 ~.
hIstory HX mild OC sx; HX trembling, sweating, great ters or performance; unable atenolol 100 mg/dayx 10 optimal dose 60 mg/day;
depreSSIve episode wIth anxIety when feeling to work or attend school weeks; Part-time Job - full appeared calmer, more
suicIde gesture observed In social or school return; still feared appropriately assertive and
performance situations deahng with strangers or confident in social sItuations
class participatIOn; had than at baseline or when on
several years of atenolol; started asking glfls
psychotherapy before for dates for first time;
medIcation trial problem controlling temper
on 75 mg/day necessitating
dosage decrease
2 30-year-old male with exceSSive sweating, tachycar- avoidance of work settings moderate response to ate- marked response in 3 weeks
continuous sx since college; dla, irregular breathing in with heavy social demands; nolo I 50 mg/dayx3 weeks, - optimal dose 45 mg/day;
recurrent mild depressions social situatIons restnctlOn of career 100 mg/dayx5 weeks; greater physical symptom
2-3 days/month opportunities moderate reduction in and social anxiety reduction
phYSIcal symptoms and than on atenolol; energy
social fear; previous trial and mood also better; gains
of hypnotherapy modestly maintained after 5 months
helpful on drug
3 30-year-old male WIth dIscomfort, mability to avoidance of SOCIal relatlOn- no benefit from imIpramine moderate response to 90 mg/
continuous sx since age 18; express himself in socml shIps outside marnage and 250 mg/day; no benefit from dayx 16 weeks; more comfort-
also had hx polydrug abuse encounters nuclear family; great inderal x 3 weeks up to able and much more WIlling to
anxiety discomfort WIth colleagues 160 mg/day plus xanax enter social situations, see
at work 0.5mg q.l.d. fnends or relatives, go to
parties. Relapsed when drug
was stopped. Similar positive
response to tranylcypromine
60 mg/dayx7 months,
followed by gradual loss of
efficacy; repeat phenelzine
trial not helpful
4 42-year-old female with frequent anxIety attacks fear of sIgning name in 4 years of group and moderate response after
20-year continuous hx of when feeling watched by pubhc, eating in public or supportive psychotherapy; several weeks on 30 mg/day
social anxiety; also mild other people, with palpita- giving talks to groups; all 9 weeks on atenolol up to WIth significantly decreased
checking rituals WIth no tions Jittenness, shortness interfere WIth the small 100 mg/day with moderate social anxiety; patient then >-'
Vl

"

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Table III. (cant.)

Pa- Background Baseline Baseline Previous Phenelzine


tient data symptoms disability therapy response C
(1)
0-
0
associated functional of breath and sweating; business owned and run benefit; less anxiety stopped drug due to dissatis- @,.
impairment blushes. and feels this is by patient symptoms when feeling faction with dietary con- N
visible to others under scrutiny, but still straints, with rapid and full
avoIded speaking to groups; relapse
symptoms returned fully
after 10 weeks off atenolol
5 34-year-old male with severe hand tremors when avoidance of luncheon or poor response to atenolol marked response on
12-year contmuous hx, and eating or writing 10 publIc; dinner dates, which 50 mg/day which made hIm drug x 12 weeks in conjunction
public speaking anxiety great subjective anxiety wIth interfered with profes- shake more and made him with contmued tranxene
going back to 'childhood' public speaking and In socIal sIOnal and personal life, feel more nervous; same 7.5 mg t.i.d.; on phenelzine
situatIOns aVOIdance of jobs with response to propranolol 60 mg/day, social anxiety
sIgnificant speaking or 10mg q.i.d.; some subjective markedly decreased; goes to
social demands benefit from propranolol restaurants 3-4 times a week
10 mg t.i.d., but still avoided with friends; much more
eating or dnnking with comfortable socially; no
others in restaurants or longer fears to sign name in
giving talks, despite public; gams maintained for
addition of tranxene 7.5 mg 5 months on phenelzine;
t.i.d. postural hypotension on
75 mg/day
6 23-year-old male wIth palpitations, tremor, SOB, very uncomfortable in any no improvement on marked response to 45 mg/day
3-years continuous sx; blushing, sweating and social encounter; no fnends imipramine 300 mg/day after 12 days on drug; Physical
initially misdiagnosed as panic anxiety in social or dating activity with combined IMIIDMI symptoms blocked - signifi-
agoraphobic with panic situations level of 444 ng/ml cantly less anxiety; insomnia
attacks - poor response to and memory problems on
imipramine led to discovery 60mg/day ameliorated with
that patient only panicked dosage reduction to 45 mg/day;
in social situations; then benefits sustained over
treated with phenelzine lOweeks on drug; equally
helped by pargyline 75 mg/day
7 24-year-old male wIth 4 sweating, distress, dizziness, avoidance of any socIal 9 months of weekly marked response after 4 weeks
years continuous sx; suicide palpitations, trembling, fear contacts besides wife; psychotherapy 10 high drug, 1 week on 60 mg/day;
gesture age 15; year-long of being watched or works at night to aVOId school significant decrease in social
major depression age 17; embarrassed; feels people people; daily alcohol use for anxiety - mood also improved;
labile personality disorder - laugh at him sleep; dropped out of now able to work day shift;
moderate marijuana use and college due to socIal anxiety able to function well without
current mild alcohol abuse; side effects x 8 weeks; stopped Ul
Hx poly-drug abuse drug - relapse after 3 weeks 00
-

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8 28-year-old female with mental confusIon, trembling, almost complete avoidance none marked response beginning
20-year continuous hx of vOIce change, Jaw and chest of relationships with men; 3 weeks after starting drug
social anxiety; beginmng as tightening, palpitations and avoidance of public (when on 60 mg/day);
VJ
fear of public speaking at blushIng in presence of men speakIng; problems with 75 mg/day resulted in marked 0
age 8; minor depressIon to whom she feels attracted, work attentuation of anxiety at O.
2 years ago following wIth public speaking, and work and when interacting e:..
medical problem when tryIng to present or sell with men; mild fluid retention '"C
::l"
and overtalkattveness at this 0
dose; dose reduced to cr
<;;.
45 mg/day with amelioration
of side effects and mainte-
nance of gains; now 10 weeks
on drug
9 44-year-old female with 19 dIffIculty wIth vOice and diffIculty audItioning as a PRN dIazepam not helpful moderate response; optimal
years contInUOUS symptoms; concentratIon, palpitations, singer; aVOIdance of dose 30 mg/day resulted In
hx recurrent unipolar sweating, and occasIonal auditions feeling calmer during
depression and PTSD diarrhea In performance auditIOns and in bUSIness
situations such as audItions transactions x 4 months
or recitals (patient was previously
unaware of difficulty in this
area); mood also improved;
unable to tolerate higher doses
10 28-year-old male with 10 Inability to concentrate, fear restricted ablhty to perform poor response to Moderate response - symptoms
years contInUOUS symptoms of humiliation, tachycardia, In graduate program - fears psychotherapy and behavior responded at 45 mg/day with
'butterfly' sensatIOn in of gOIng to lectures, therapy; no response to decreases in self-consclOus-
abdomen, hand tremors in speaking in class; very placebo in 8-week double- ness, antIcipatory anxiety and
public speakmg and fearful of askIng women for blind trial phYSIcal symptoms. Insomnia
especially In dating situa- dates, with markedly and day time drowsiness
tions restricted dating pattern forced dosage to Ineffective
levels
11 37-year-old male WIth sweaty palms, tachycardia, dread and aVOIdance of any stress management course, marked response to phenelzine
marked public speaking palpItatIOns, flushIng, public speakIng situation 4 VISItS to psychologist up to 60 mg/day for 10 weeks;
anxiety since telling his light-headedness, pares- whIch limited ability as a without benefIt; valium no longer fearful or uncom-
parents of homosexuahty thesias; fears loss of control, consultant somewhat helpful; fortable when makIng
9 years pnor; also fear of embarrassment or humilia- atenololx4 weeks up to business presentations
elevators and one panic tion; fears he will reveal 100mg/day of no benefit
attack 3 years pnor on a himself in public to be a
bridge wIth subsequent homosexual
avoidance of bridges; also
current GAD symptoms

>-'
U>
'C!

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Liebowitz 160

Previous treatment varied. Patients 1-5 and 11 received beta-blockers


with moderate to no benefit before trying phenelzine. Patients 3 and 6
failed to benefit from vigorous trials with imipramine.
As indicated in table III, 7 of 11 patients showed marked improve-
ment with phenelzine, while the remaining 4 experienced moderate be-
nefit. Response was usually manifest 3-4 weeks after starting the drug,
and at doses of 45-60 mg/day. Physical accompaniments of social anxiety
disappeared, and patients became significantly more comfortable and out-
going in vocational and social settings. The most dramatic example of this
involved patient 1, who had been so afraid to attend school or socialize
with peers before treatment that he was virtually housebound. On phenel-
zine he not only attended school regularly and obtained a part time job,
but started spending time with male fellow students and asking female stu-
dents for dates.
Interestingly, optimal phenelzine dose was 45 mg or less a day in 6 of
11 patients, with uncomfortable side effects such as insomnia, memory
problems, irritability, sexual dysfunction, overstimulation and edema oc-
curring at higher doses. Phenelzine was quite acceptable to most patients,
although 2 (patients 4 and 7) stopped because of dietary restrictions de-
spite benefit, and 1 (patient 10) because of side effects.
Course of therapy ranged from several weeks to seven months with no
diminution of gains as long as phenelzine was continued. A repeat trial in
patient 3, however, was not helpful. Of 4 patients (patient 3,4,7,10) who
stopped MAOls at least transiently, all experienced relapses.
The MAOI-tricyclic comparisons in outpatient depressives also
suggest phenelzine efficacy in reducing social anxiety and social discom-
fort. Liebowitz et al. [47] found phenelzine superior to both imipramine
and placebo at 6 weeks on the interpersonal sensitivity (social discomfort)
and paranoia (touchiness, not psychosis) SCL-90 scales in atypical depres-
sives. Inclusion criteria for atypical depression included meeting RDC for
major, minor or intermittant depression, maintaining mood reactivity (the
ability to be at least transiently cheered by pleasant events), and two or
more of the following four associated features: overeating, oversleeping,
extreme fatigue or lethargy, and chronic hypersensitivity to rejection. Nies
et al. [75] also found phenelzine superior to amitriptyline on the SCL-90
anxiety and interpersonal sensitivity scales in outpatient depressives. In
both studies, interpersonal sensitivity was a better measure than depres-
sion for distinguishing between MAOI and tricyclic effects, suggesting a
primary phenelzine effect on social discomfort.
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Social Phobia 161

This is especially interesting since it contradicts the assertion of Marks


et al. [76] that antidepressants have efficacy in anxiety disorders only by
relieving associated dysphoric or depressive features. Some social phobics
have no history of affective disorder at all. Those that do remain socially
phobic during depression-free periods as well, suggesting that, for them,
affective syndromes are secondary. This is in contrast to patients who be-
come socially avoidant only during affective episodes who therefore do not
meet DSM-III social phobia criteria. The unremittingly depressed, chron-
ically socially avoidant patient does, however, present a problem in diffe-
rential diagnosis.

B-Adrenergic Blockers
The only reported placebo-controlled study of beta-blockers in social
phobics involved 16 patients, all of whom concomitantly received social
skills training [71]. Patients were randomized to propranolol hydrochlo-
ride or placebo, and propranolol dose adjusted to lower heart rate to 60
beats/min. Specific dosages are not reported. No significant differences
were noted between the 6 patients who received propranolol and the 6 pa-
tients who received placebo who completed the trial. Limitations of this
study include small sample size, lack of specific diagnostic criteria, lack of
controls and blind ratings for social skills training, and the fact that four
patients had panic attacks. These panic attacks are not described; if they
were spontaneous, they complicate the clinical picture, since spontaneous
panic attacks respond poorly to beta-blockers [34-38]. Further, if these 4
patients had social anxiety secondary to the panic attacks, then they would
not meet DSM-III criteria for social phobia.
Numerous analogue studies have examined the effect of beta-blockers
on anxiety during observed performance in nonpatient samples, which
shares many features with social anxiety in patient samples, including
symptom pattern and evoking situations. Of 11 controlled trials [23-33], 8
found a beta-blocker superior to placebo in reducing some aspect of per-
formance anxiety, while 3 others found no overall difference (table IV).
Since the majority of these studies involved administration of short-term
doses prior to a performance situation, the findings are most relevant for
those social phobics who experience only occasional and predictable anx-
iety episodes, such as with public speaking or audition anxiety. For those
social phobics whose symptoms occur more frequently or in less easily pre-
dicted situations, continuous treatment is more appropriate, and con-
trolled studies of maintenance regimens of B-blockers are needed.
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Liebowitz 162

Table IV. Controlled trials of beta-blockers: studies of performance anxiety in non clinical popula-
tions

Source Sample Design Dosage Final


drug type outcome

Liden and Gottfnes 15 musIcian volun- double-blind alprenolol 50 and posittve: alprenolol
[23] teers from among companson of 100 mg; nonselective effects on palpitations,
the most symptom a- single-dose al- beta-blockers mcreased muscle tone,
ttc members of a prenolol and and tremor greater
professional sym- placebo, each taken than for placebo
phony orchestra before 2 concerts
Gottschalk et al nonanxlOUS college double-blind propranolol hydro- negative: acttve drug
[24] volunteers companson of chlonde 60 mg in effect m lowenng
short-term pro- divided doses over anxiety pnor to, but
pranolol hydro- 12-14 h prior to not dunng, interview
chloride or placebo testmg; nonselective
on response to beta-blockers
stressful mterview
Knshan [25] 32 college students; double-blind oxprenolol 40 mg posittve: only ox-
selection criteria not companson of tWice a day; prenolol group showed
stated mamtenance dose of diazepam 2 mg twice better than predicted
oxprenolol or a day; nonselective exmination perfor-
diazepam on beta-blockers mance; only diazepam
examinatIOn group expressed
performance subjective Sense of
performance improve-
ment; no statistical
comparisons given
Siitonon and J anne 17 amateur bowlers double-blind oxprenolol 40 mg; negative: no overall
[26] comparison of nonselective difference between
smgle-dose ox- beta-blockers group; oxprenolol
pre nolo I or placebo helpful to subgroup of
on bowhng compett- bowlers (one-third of
tlOns sample) with high
heart rate; 50% of
oxprenolol sample
bowled worse with
drug than with placebo
James et al. [27] 24 volunteer stnng double-bhnd oxprenolol 40 mg; posittve: less subjective
musician players crossover compari- nonselective nervousness and
son of smgle-dose beta-blockers better objective
oxprenolol and performance With
placebo taken before oxprenolol
solo performance
Brantigan et al. 29 volunteer double-blInd propranolol hydro- pOSItIve: subjectIve
[28] musicians crossover compao- chloride 40 mg; anxiety, physical
son of smgle-dose nonselective symptoms, and
propranolol and beta-blockers perfonnance better
placebo taken before with propranolol
mUSical performance
Neftel et al. [29] 22 volunteer string double-blind parallel atenolol 100 mg; positive: atenolol
musicians group comparison of cardlOselective group showed less
smgle-dose atenolol beta-blockers stress, fnght, and
and placebo taken performance impau-
before performance ment m front of
With and Without an audience than did
audience placebo; effects
statistically weak
Krope et al. [30] 104 student volun- double-blind parallel mepmdolol 5 or negative: no drug
teers group companson of 10 mg; nonselective placebo differences
single-dose me pin- beta-blockers found for subjective
dolol or placebo with anxiety or test
rea1 examinations performance
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Social Phobia 163

Table IV. (cont.)

Source Sample DesIgn Dosage FInal


drug type outcome

Hartley et al. [31] sample 1: 16 student double-blInd propranolol hydro- posItIve: propranolol
volunteers WIth hIgh crossover of chlorIde 40 mg; had slgmficantly
anxIety scores short-term prop- nonselectIve greater effect on
ranolol and placebo, beta-blockers self-report and
each taken before observed anxIety than
publIc speakIng placebo
sample 2: 17 student same as above same as above propranolol more
volunteers WIth hIgh effectIve than placebo
anxIety scores and 12 In reducIng observed
WIth low scores performance anxIety
In the hIgh anxIety
group
James et al. [32] 30 professIOnal double-blInd pIndolol 5 mg; positIve pmdolol
musicians crossover of nonselectIve more effectIve than
SIngle-dose pIndolol beta-blockers placebo on anxIety,
and placebo taken pmdolol caused
before recItals subjectIve, but no
objectIve Improvement
In mUSIcal performance
DesaI et al. [33] 44 normal student experIment 1: diazepam 5 mg; negatIve: diazepam
volunteers structured dIazepam or placebo oxprenolol 80 mg; Improved performance
IOtO hIgh and low double-blind parallel nonselectIve more than placebo 10
anxIety groups group dosage; beta-blockers high anxIety group; no
experIment 2: oxprenolol-placebo
oxprenolol or dIfferences noted
glacebo 10 double-
lind parallel group
deSIgn; memory task

Ten of the 11 studies outlined in table IV involved nonselective beta-


blockers. The study by Neftel et al. [29], however, used atenolol, a car-
dioselective beta-blocker that penetrates the central nervous system far
less well than propranolol [77]. In addition to the lower incidence of cen-
tral nervous system side effects reported for atenolol, demonstration of ef-
ficacy in social phobia may support peripheral rather than central au-
tonomic mediation.

Atenalal Study. To test the efficacy of continuous therapy with a car-


dioselective beta-blocker, 10 patients meeting DSM-III for social phobia
were openly treated with atenolol up to 100 mg/day [73].
Of the 10 patients, 6 were male and 4 were female. Age range for all
10 patients was 19-54 years (mean, 33.5 years). At onset, median age was
18 years and mean age, 21.9 years.
A range of situations triggered these patients symptoms. At one end
of the spectrum were very specific phobic stimuli, such as giving a speech
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Liebowitz 164

in public. At the other end were global fears of almost all social encoun-
ters, even to the point of fearing being on an elevator with other people.
The former patients appeared closest to the traditional form of perfor-
mance anxiety.
In all cases, including those bordering on simple performance anxiety,
social phobia led to significant functional impairment. Patients experi-
enced a restriction in career advancement, inability to attend school, dif-
ficulty maintaining friendships, and fear of romantic relationships. Five
patients abused alcohol and one had a history of poly-drug abuse, includ-
ing significant benzodiazepine abuse.
Five had histories of at least one depressive episode. One had made
a suicide gesture and another had a severe psychotic depression about 1
year before the study. Other concomitant psychiatric problems included
two patients with generalized anxiety disorder and one patient each with
obsessive-compulsive disorder and hypochondriasis. At the time of enter-
ing the study none met DSM-III criteria for major depressive disorder, al-
coholism, schizophrenia, or bipolar affective disorder.
As part of the routine medical screening, it was first determined that
all 10 subjects had no history of asthma, bronchial disease, diabetes mel-
litus, or cardiovascular disease except uncomplicated mitral valve pro-
lapse. All had normal EeGs. Patients were then started on atenolol, 50
mg/day, in one morning dose. They were instructed to take their pulse
every day and to withhold medication and call the clinic if their heart rate
dropped below 50 beats/min.
If after 1 week there was no significant improvement in the patient's
condition and pulse rate was above 50, atenolol was raised to the
maximum recommended dose of 100 mg/day, also in a single morning
dose. Patients were then followed for at least 5 more weeks at this level.
Response to medication was judged to be 'marked' if both patient and
treating psychiatrist agreed that almost all symptoms of social anxiety and
phobic avoidance were relieved. Such patients became able to comfortably
enter the phobic situation at will with minimal discomfort. Response was
judged 'moderate' if the patient reported significant improvement in abil-
ity to enter phobic situations, but some degree of anxiety and apprehen-
sion persisted. Although now able to enter previously avoided situations,
such patients still experienced discomfort and a tendency to wish to avoid
some situations. Finally, if there was no clinically significant reduction in
anxiety or phobic avoidance (which included slight benefits), the response
was judged 'absent'.
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Of the 10 social phobic patients who completed at least 6 weeks of


treatment, 5 had 'marked' response to atenolol, 4 had 'moderate' re-
sponse, and only one had 'absent' response. Seven of the 10 patients took
100 mg of atenolol daily, although one of these developed bradycardia at
the higher dose and was lowered to 50 mg daily. The other three patients
improved on doses of only 50 mg daily.
Side effects were surprisingly minimal. Two subjects complained of
fatigue and lowered energy, although not enough to impair functioning or
require dose adjustment. Another patient reported a 'fainting spell' while
on 50 mg of ate nolo I and the drug was discontinued. However, the patient
clearly did not lose consciousness during this episode and never had re-
corded pulse rates below 50. The exact nature of the incident could not be
determined. The patient with mild bradycardia improved moderately, and
the one who reportedly fainted improved markedly on atenolol.
Response to beta-blockers may discriminate social phobics from pa-
tients with panic disorder or agoraphobia with panic attacks. While beta-
blocker therapy in patients with agoraphobia or panic disorder has been
only preliminarily assessed, available evidence suggests a lack of efficacy.
Hafner and Milton [38] found mixed effects on a single-dosage trial. Noyes
et al. [36] found diazepam (which itself is not too useful) superior to pro-
pranolol in a 4-week double-blind crossover study involving 21 patients
with panic disorder or agoraphobia. Heiser and DeFrancisco [37] found
that small doses of propranolol given for up to 2 weeks did not block panic
attacks associated with agoraphobia. Also, acute intravenous propranolol
pretreatment, which produced marked peripheral B-adrenergic blockade,
did not block either the anxiety or tachycardia of lactate-induced panic at-
tacks [34].

Other Drugs
There is a paucity of studies of tricyclics in social phobics. Two open
[68, 69] and one controlled study [70] have reported clomipramine hydro-
chloride efficacy in mixed samples containing social phobics but did not
report outcome separately for the social phobics. In two recent MAO 1-
tricyclic studies of nonendogenous depression, tricyclics were less effective
than MAOIs in reducing social anxiety [46, 75]. Klein [personal commun.,
1984] also found no evidence of imipramine efficacy among the social
phobics included in his simple phobia group [9].
To our knowledge, benzodiazepines have not been studied in social pho-
bics. In analogue samples, the evidence for efficacy is not robust [25, 33].
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Controlled drug trials of social phobics (and other psychiatric dis-


orders) should involve PRN short-term response, maintenance, and dis-
continuation phases. PRN and trials of 6-8 weeks' duration answer the
question of short-term efficacy. Maintenance trials, where responders to
short-term trials continue double-blind to receive their study drug for an
additional 6 weeks to 6 months, reveal whether further improvement oc-
curs with longer treatment and whether short-term responses are durable
or transient when medication is continued. Double-blind, randomized,
placebo-controlled discontinuation of drug responders after 3-6 months of
treatment shows whether continued drug is needed to maintain therapeu-
tic gains. Drug trials should also involve long-term follow-up to assess
incidence of relapse following drug withdrawal.

Behavioral Treatment of Social Phobia


Behavioral treatment of social phobics has been the subject of recent
reviews [42, 43, 61, 78-86] and will be briefly summarized. The three
principal forms of treatment found useful in controlled studies are de-
sensitization or exposure, social skills training, and cognitive restructur-
ing.
After an extensive review, Emmelkamp [42] concluded that while sys-
tematic desensitization had consistently been effective in the treatment of
social anxiety in analogue populations, it had limited value in clinical sam-
ples of social phobics. In contrast, a study by Shaw [81] comparing desen-
sitization, flooding, and social skills training found similar 'useful
therapeutic gains', for all three treatments in a clinical population of social
phobics.
Several controlled studies have demonstrated the superiority of social
skills training over systematic desensitization for socially anxious individu-
als [42]; others did not find consistent differences [57, 81, 82]. As noted by
Brady [61, 79], controlled studies of social skills training in psychiatric out-
patients have usually involved loosely defined samples with 'social in-
adequacy' or deficient social skills rather than rigorously classified social
phobics.
One exception is the previously mentioned study by Shaw [81] that
compared the effects of desensitization, flooding, and social skills training
on 30 social phobics and found no differences among treatments. Another
is a study by Stravynski et al. [83] that compared social skills training and
social skills plus cognitive modification in social phobics and found both
helpful, with no differences between treatments. Since neither study had
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Social Phobia 167

a no-treatment control, the reported therapeutic gains cannot be specifi-


cally attributed to the treatments.
Cognitive therapies have been found helpful in reducing social anxiety
[84], test anxiety [85], and speech anxiety [86] in analogue populations.
Studies of cognitive therapy in clinical social phobics, however, are lack-
ing.
Cognitive restructuring was found superior to desensitization and to a
waiting list central in reducing symptoms in socially anxious community
volunteers [58]. Kendrick et al. [87] found cognitive therapy and be-
havioral rehearsal more effective than a waiting list control for severe mu-
sical performance anxiety assessed during a demanding live performance
during follow-up after treatment. This is especially interesting because
there were no differences between baseline and immediate post-treatment
evaluations of studio based performance. At follow-up, patients who re-
ceived the two active treatments appeared less anxious, showed greater
improvement in quality of playing and had more positive self appraisal.
Butler et al. [88] recently found exposure plus anxiety management
training superior to exposure plus a control 'associative therapy' for social
phobics, particularly on the Social Avoidance and Distress (SAD) and
Fear of Negative Evaluation (FNE) measures of distress caused by, and at-
titudes toward, social interaction. Anxiety management training involved
the three techniques of relaxation, distraction and rational self-talk. Butler
[89] has also recently discussed in detail the problems of applying exposure
techniques to social phobics. In her view, supplemental anxiety manage-
ment training is helpful in treating the cognitive aspects of social phobia,
particularly, the fear of negative evaluation.
It needs to be better established whether behavioral techniques result
in substantial, and lasting, therapeutic gains when administered to clini-
cally ill social phobics. On the hopeful side, in the study by Shaw [81] seri-
ously incapacitated patients are described after treatment as coping better
with jobs that had previously stressed them and many were able to extend
their social activities. Further, these gains were maintained over a 6-month
follow-up period.
It is also uncertain whether the various behavioral treatments have
specific or nonspecific antidemoraiizing effects. That is, is desensitization
specifically effective in patients with histories of prior traumatic social or
performance experiences, and social skills training most useful for patients
deficient in social skills? Or are the various behavioral therapies equally
effective in social phobics regardless of preexisting history or baseline
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Liebowitz 168

deficit? Ost et al. [80] have found that social skills training may be more
effective for 'behavioral reactors' and applied relaxation more effective for
'physiological reactors' among social phobic samples.
Once the pharmacological and behavior therapy response patterns of
social phobia are elucidated, the comparative and interactive effects of
drug and behavior therapy will require assessment. Other forms of
psychotherapy may also be of use but have not been systematically asses-
sed.

Conclusion

Social phobia appears distinct from other phobic subtypes in terms of


demographic and clinical features. The disorder is not uncommon and
tends to be chronic and at times disabling. Alcoholism and depression are
common associated syndromes. Analogue and open clinical studies
suggest efficacy for B-adrenergic blockers, while open clinical trials and
co~trolled studies in mixed phobic populations suggest MAOIs may be of
benefit. Open and controlled trials also support at least some efficacy of
behavioral therapies, including exposure, social skills training and cogni-
tive approaches. However, lasting effects of all treatments remain to be
demonstrated.
Major uncertainties also exist concerning the definition, classification,
prevalence, severity, etiology, pathophysiology, assessment, and treat-
ment of social phobia. While social phobia has received some attention
from British investigators, it has been, until very recently, neglected in the
mental health literature, except by behavior therapists. Interest in social
phobia among clinicians and researchers is starting to grow, however, as
specialized anxiety clinics proliferate.
This offers a number of exciting opportunities. For one, while social
phobics appear quite disabled, they may also be responsive to treatment,
offering an opportunity for refined diagnostic and decisive, specific,
therapeutic action. In this regard, social phobia may prove similar to cer-
tain depressive syndromes, or to panic disorder or agoraphobia with panic
attacks.
Second, social phobics allow an important comparison group for de-
velopmental, biological, and treatment studies of other anxiety patients,
particularly agoraphobics. Studying more than one phobic group provides
a needed perspective when differences are found between a particular
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Social Phobia 169

phobic subtype and normal controls, permitting determination of whether


the differences are specific to that patient group or pertain to anxiety pa-
tients in general.
Social phobia also offers a fertile field for the study of the interaction
of developmental, biological and psychological factors, both in terms of
pathophysiology and treatment. Preliminary investigations suggest that
both cognitive factors and biological hyper-reactivity contribute to social
phobic symptoms. The unusually high prevalence of men in this group, as
well as the social clumsinesses require investigation of possible minimal
brain dysfunction. Uncertainties in this area are illustrated by the confu-
sion surrounding the relationship of social phobia to avoidant personality
disorder.

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Michael R. Liebowitz, MD, New York State Psychiatric Institute,


722 West 168th Street, New York, NY 10032 (USA)
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