SOCIAL ANXIETY DISORDER
(SOCIAL PHOBIA)
AND
SELECTIVE MUTISM
Samuel J. Eckrich, M.S.
Child Psychopathology
University of Central Florida
BACKGROUND AND HISTORY OF SOCIAL ANXIETY
DISORDER (SOCIAL PHOBIA) (SAD)

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400 BC: “…He dare not come in company for fear he
should be misused, disgraced, overshoot himself in
gesture or speeches, or be sick; he thinks every man
observes him.” –Hippocrates
1900-1950: “Social neuroses”
“Social Phobia” included in the DSM-III (1980, defined in
1987).
Recognized in children in DSM-VI (1994)
Renamed “Social anxiety disorder (social phobia)” in
DSM-V.
DIAGNOSTIC CRITERIA FOR
SOCIAL ANXIETY DISORDER
(SOCIAL PHOBIA)
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A. Marked fear or anxiety about one or more social situations in which the
individual is exposed to possible scrutiny by others. Examples include
social interactions (e.g., having a conversation, meeting unfamiliar people),
being observed (e.g., eating or drinking), and performing in front of others
(e.g., giving a speech). Note: In children, the anxiety must occur in peer
settings and not just during interactions with adults.
B. The individual fears that he or she will act in a way or show anxiety
symptoms that will be negatively evaluated (i.e., will be humiliating or
embarrassing; will lead to rejection or offend others).
C. The social situations almost always provoke fear or anxiety. Note: In children,
the fear or anxiety may be expressed by crying, tantrums, freezing,
clinging, shrinking, or failing to speak in social situations.
D. The social situations are avoided or endured with intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual threat posed by the
social situation and to the sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or
more.
DIAGNOSTIC CRITERIA FOR
SOCIAL ANXIETY DISORDER
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G. The fear, anxiety, or avoidance causes clinically significant distress
or impairment in social, occupational, or other important areas of
functioning.
H. The fear, anxiety, or avoidance is not attributable to the physiological
effects of a substance (e.g., a drug of abuse, a medication) or
another medical condition.
I. The fear, anxiety, or avoidance is not better explained by the symptoms
of another mental disorder, such as panic disorder, body
dysmorphic disorder, or autism spectrum disorder.
J. If another medical condition (e.g., Parkinson’s disease, obesity,
disfigurement from burns or injury) is present, the fear, anxiety, or
avoidance is clearly unrelated or is excessive.
Specify if: Performance only: If the fear is restricted to speaking or
performing in public.
CHANGES IN DSM-V
1) Social phobia = Social Anxiety Disorder (Social
Phobia).
2) The person does not have to recognize that
their fear is unreasonable/disproportionate.
3) Specifier of “Generalized” replaced with
“Performance Only” due to
operationalization issues.
ASSOCIATED FEATURES
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Inadequately assertive, excessively submissive
Inadequate eye contact, rigid posture, overly soft
voice
Socially delayed- live at home longer.
Seek out jobs that do not require contact (not
“performance only” group.
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Self medication is common (adolescents)
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Increased heart rate. Blushing.
DIFFERENTIAL DIAGNOSES
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Pretty much everything
Normative shyness, agoraphobia, panic disorder,
anxiety disorder, selective mutism, separation
anxiety, specific phobias, major depressive
disorder, body dysmorphic disorder, delusional
disorder, autism spectrum disorder,
personality disorder (avoidant), eating
disorders, obsessive compulsive disorder,
schizophrenia, ODD, cultural norms.
Children (7-12 y.o.) and Adolescents (13-17 y.o.) often
have differential presentation (Rao et al., 2007):


Children have a broader general pychopathology
Adolesc. have a more pervasive pattern of social dysfunction
ANXIETY-INDUCING SITUATIONS
CHILDREN VS. ADOLESCENTS
Rao, Beidel, Turner, Ammerman, Crosby, Sallee, 2007
PREVALENCE/AGE OF ONSET
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12 month: 5-8% (Costello et al. 2003; Kessler et al. 2012; Wittchen et al. 1999).
Lifetime: 7-13% which makes it the 3rd most common
psychiatric disorder (Kashdan & Herbert, 2001)
Child/Adult rates are similar but typically decrease with age
(Wolitzky-Taylor et al. 2010)
More common in females (1.5M:2.2F), especially adolescents
Lifetime ~10% for females
~5% for males (Wittchen, 1999)
Higher for American Indians, and lower for Asian, Latino,
African American compared to non-Hispanic white
(Lewis-Fernández et al. 2010)

Median age of onset is 13. 75% between 8-15.
(Kessler et al. 2005).
RATES OF COMORBIDITY
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Any other disorder (81%)
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Any anxiety disorders (50%)
(McGee et al., 1996)
(Wittchen et al., 1999)
- Panic disorder (5-10%)
- Agoraphobia (7-12%)
- Specific Phobias (40-50%)
-Suicide attempts (14.3%) (Cougle et al., 2009)
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Depressive disorders (30-50%)
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Substance use disorders (35-45%)
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Females: More likely to have comorbid depressive, bipolar,
and anxiety disorders.
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Males: More likely to fear dating, have ODD, and CD, and
use Substance Use Disorders.
(Wittchen et al., 1999)
(Wittchen et al., 1999)
(Ruscio et al. 2008; Turk et al. 1998).
* Generally difficult to ascertain because shyness is associated with other
anxieties, depression, and general neuroticism. (Rapee and Spence 2004).
SECONDARY DIAGNOSES FOR CHILDREN
VS. ADOLESCENTS
Rao, Beidel, Turner, Ammerman, Crosby, Sallee, 2007
SELF REPORT MEASURES CHILDREN VS.
ADOLESCENTS
HERITABILITY
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Moderate but significant genetic influence
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.31-.65 heritability estimate (anxiety disorders) (Albano et al., 1995; Beatty et al., 2012)
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.34-.66 for behavioral inhibition (Robinson et al., 1992)
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.48 for “shyness” and “fear of negative evaluation”
(Stein et al., 2002)
* Still difficult to know what is specifically attributable to SAD:
high interrelationship of genetic influences on other
anxieties, depression, and SUDs
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One study found that in a study 1198 twins, the best-fitting model
indicated as much as 13% of the variance in social fears was
accounted for by genetic factors unique to this type of fear.
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Specific genetics associated with different types of fears
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Stein et al., 2001a, 2001b, finds a common genetic influence
for both SAD in adolescents and depression in adulthood.
GENETICS RELATED TO
NEUROTRANSMITTERS
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Repeat polymorphisms in genes associated with:
Dopamine transporters (DAT) (Rowe et al. 1998)
 Serotonin Transporters (5-HTT) (Schmidt et al., 2002)
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However:

There just as many studies that do not find links.
(Kennedy et al., 2001, Stein et. al 1998)
DAT and 5-HTT are commonly dysregulated in most
psychiatric disorders
 Maybe Genome Wide Association studies (GWAS)
will offer specificity in the near future

DSM-V INFORMED MODEL
Genetics
Environment
Social Anxiety
Disorder
Temperament
Gender
ENVIRONMENTAL ETIOLOGY OF SAD
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Direct traumatic conditioning
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92% of SAD adults had a history of teasing
compared to 50% with Panic Disorder and 35% with
OCD (McCabe et al., 2003)
56% of those with specific social phobias had a direct
link to a traumatic event (Stemberger et al., 1995)
ENVIRONMENTAL ETIOLOGY OF SAD
CONT.
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Social Learning Theory
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Vicarious conditioning:
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Ex. Watching a classmate being humiliated in class. 13%
blamed vicarious conditioning event
Avoidance behavior modeling:
Individuals with SAD are more likely to have parents who
exhibited avoidant behavior (Rapee and Melville, 1997)
 Reciprocation of avoidant behavior (Barrett et al., 1996)
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Cultural transmission
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“Taijin Kyofusho” - Japanese analogue of SAD engendered
by a collectivist society.
ENVIRONMENTAL ETIOLOGY OF SAD
CONT.
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Preparedness Theory (Ohman et al., 1985)
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Evolutionary perspective in which the dominance
hierarchies that signal intrapersonal threats
inherently produce fear (become CSs)

Paired angry faces with mild shock and showed that
that the conditioning was superior to that of happy
faces.
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Even worked when faces were shown subliminally
(Esteves et al. 1994)
ENVIRONMENTAL ETIOLOGY OF SAD
CONT.
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Perception of Uncontrollability
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Social defeat in animals
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Drug studies
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Uncontrollable shock increases submissiveness (Williams
and Lierle, 1987)
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Contributes to individual differences and risk factors
TEMPERAMENTAL ETIOLOGY OF SAD
CONT.
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Behavioral Inhibition (BI)
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A Temperamental diathesis for SAD.
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Similar to Specific Phobias, underlying individual
differences may account for the development of SAD
Many people have traumatic experiences without ever
developing anxiety. This could be due to experience,
Presence of BI can reliably predict the onset of specific
phobias in childhood and SAD in adolescence (Haywood et al., 1996;
Kagan et al., 1997)
REVIEW OF ENVIRONMENTAL RISK
FACTORS
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Direct traumatic conditioning
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Vicarious conditioning
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Avoidance behavioral modeling
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Cultural transmission
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Preparedness theory (evolutionary)
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Perception of uncontrollability
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Temperamentally predisposed (Behavioral Inhibition)
BEHAVIORAL INHIBITION (BI)
EXPERIMENTAL DESIGN
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Kagan, Reznick, and Snidman 1987. “Hypothesis: Individual
differences in behavioral reactions to threat and challenge is
due to threshold differences in circuits… influenced by the
hypothalamus.”
Screened 400 children by phone and observation to find 60
consistently inhibited and 60 consistently uninhibited.
Basically measures of shyness.
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Two groups of 60 equal 1M:1F.
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Measurements taken at 21 months, 31 months, 3.5 yr, 4 yr, 5.5yr.
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Unfamiliar female examiner, unfamiliar toys, separation from
mother, unfamiliar peer of both sexes, classmates, cognitive
tests, stressors, objects suggestive of risk (balance beams, black
box with a hole).
BI = latencies to interact, immediate retreat, proximity to mother,
cessation of play or vocalization
BI PRESERVATION OF BEHAVIOR
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Those inhibited at 21 months were significantly
correlated to those at 5.5yrs (r = .52). Likewise
from 4-5.5yrs (r = .67).
Latency to speak was the
most sensitive measurement
of BI
*More preservation of
uninhibited than
inhibited
*More boys than girls
changed from inhibited to
uninhibited
CORTISOL
PHYSIOLOGICAL MEASURES
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Heart rate, pupil dilation, muscle tension, cortisol
Inhibited
Uninhibited
Heart Rate
High and Stable
Low or Variable
Pupil dilation
Larger
smaller
Muscle tension
Increased
decreased
Cortisol
Increased
Decreases
Neurological correlates: Limbic system, HPA, reticular
activating system, nucleus ambiguous, sympathetic
nervous system (norepinephrine)
Cortisol was the best predictor of inhibited vs.
uninhibited (78%).
INITIAL CONCLUSIONS
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Behavioral inhibition is moderately preserved across time points
and physiological measures.
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State of uncertainty has physiological correlations.
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Possibly due to different thresholds of reactivity in the amygdala
and hypothalamus of inhibited vs. uninhibited children.
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Still, not every inhibited child stayed inhibited.
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Only significant when analyzed categorically, not dimensionally.
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Only 1/3 of the inhibited at 21mo. scored high on each measure.
Experience factors?
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Heritability (.34-.66) is moderately high, but still missing some
pieces: gender, parental temperament?
Make does this mean for Social Phobia? Lifetime trajectory?
RECENT BEHAVIORAL INHIBITION
STUDIES
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Schwartz, Snidman, Kagan, 1999
RECENT META-ANALYSIS OF BEHAVIORAL
INHIBITION
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Clauss and Blackford, 2012
 BI was associated with a greater than sevenfold increase in
risk for developing SAD (Odds ratio = 7.59).
FUNCTIONAL AMYGDALA CONNECTIVITY IN
BI YOUNG ADULTS
19 high BI/19 low BI in childhood were tested at 1821 (Roy et al., 2014).
 Less functional connectivity between amygdala and
striatum, pFC, insula, and cerebellum in BI.
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REVIEW THE RISKS
1. Genetics (many shared genes, possibly some specific to
social anxiety)
2. Environment (traumatic events, culture, experience,
preparedness, parental stress)
3. Temperament (Behavioral Inactivation)
4. Physiology, brain structure, neurochemicals
Genetics and Environment work together to create a
temperament. That temperament is highly correlated to
physiological changes specific to fear and stress circuitry in
the brain.
Yet, all of the variance is not assumed. Many children aren’t at
the extremes of the measurements. What other distinctions
may help identify at risk children?
SOCIAL ANXIETY AND SOCIAL
COGNITION
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“Biases and distortions in social-information processing
and thoughts may affect attitudes and beliefs that
trigger and/or maintain social phobic behaviors”
(Rapee et al., 2014)
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Ability to understand other’s mental states Clark and McManus
(2002)
Social inference (TASIT)
 Theory of Mind (Reading Mind in Eyes Test, Faux Pas )
 Identify emotions
 Questionnaires/Other tests
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Interpretation of external social events
 Reduced Processing of External Social Cues and Enhanced SelfFocused Attention
 Detection and recall of negative social cues
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WILLIAMS SYNDROME VS. SAD FMRI
VIEWING FACES: A META-ANALYSIS
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Binelli et. al., 2014
COMPARISON OF CHILDREN AND ADOLESCENTS
ON BEHAVIORAL ASSESSMENTS AND
PERFORMANCE SKILL
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Rao, Beidel, Turner, Ammerman, Crosby, Sallee, 2007
This suggests that children have generally poorer
social skills which may lead to negative cycles.
REVIEW THE RISKS
1. Genetics (many shared genes, possibly some
specific to social anxiety)
2. Temperament (Behavioral Inactivation)
3. Environment (traumatic events, culture,
experience, preparedness, parental stress)
4. Physiology, brain structure, neurochemicals
5. Social cognition and social skills
Other mediators
* Gender (adolescent)
* Maternal stress (Parent/child interaction)
THERAPY
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Division 53:
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“Coping cat” developed by Phillip C. Kendell
Children (6-13yrs) version and adolescent version (C.A.T.).
 Manual-based CBT treatment
 Participant youth are taught features of the disorder
 Develop a plan to cope with anxiety (“FEAR plan”).
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Feeling frightened
Experiencing bad things
Actions that will help
Results and rewards
Provide situations to practice plans
 Learn cues for becoming anxious and cue for using social
skills
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THERAPY CONT.
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Social Effectiveness Therapy for Children and
Adolescents (SET-C)
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Developed by Dr. Beidel
Group social skills training
Structured peer generalization sessions
Individualized behavioral exposure tx.
PHARMACOTHERAPY
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SSRIs are the most studied and effective (Reinblatt et al., 2007)
SNRI
*Adverse: Paroxitine = 2x as much insomnia, decreased
appetite, and vomiting.
Venlafaximine = weight loss
SET-C VS SSRI

Beidel et al., 2007
More efficacious than
Fluoxetine (p < .025).)
and placebo (p < .001) at
12 wks.
SET-C VS. SSRI CONT.
Also: SET-C was the only treatment superior to placebo in
terms of improving social skills, decreasing anxiety in
specific social interactions, and enhancing ratings of
social competence. But, meds are more
transportable!
NEW DIRECTIONS
Still 25-35% do not get better with any tx. (Connolly et al., 2001)
 Using virtual reality to treat and to assess (An Doan)

Genetics
Neurobiological
factors
SSRIs/
SNRIs
Gender
Temperament
Social Anxiety
Disorder
Social
Cognition/Skills
Traumatic
events, culture,
uncontrollability,
preparedness,
parental stress
SET-C/
CBT
BACKGROUND AND HISTORY OF
SELECTIVE MUTISM
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1877, German physician Adolph Kussmaul, “aphasia
voluntaria”
1980: Added to DSM-III, “Elective mutism”
Predisposing disorders were originally: Overbearing
parents, mental retardation, and trauma. NOT
connected to social phobia.
DSM-IV (1994) Changed to “Selective mutism” and
connected to anxiety disorders.
DSM-V: "Disorders Usually First Diagnosed in Infancy,
Childhood, or Adolescence" to the section for anxiety
disorders.
DIAGNOSTIC CRITERIA FOR
SELECTIVE MUTISM (SM)
A. Consistent failure to speak in specific social situations in
which there is an expectation for speaking (e.g., at school)
despite speaking in other situations.
B. The disturbance interferes with educational or occupational
achievement or with social communication.
C. The duration of the disturbance is at least 1 month (not limited
to the first month of school).
D. The failure to speak is not attributable to a lack of knowledge
of, or comfort with, the spoken language required in the
social situation.
E. The disturbance is not better explained by a communication
disorder (e.g., childhood-onset fluency disorder) and does
not occur exclusively during the course of autism spectrum
disorder, schizophrenia, or another psychotic disorder.
Diagnostic and Statistical Manual of Mental Disorders(5th ed.,
CHANGES IN DSM-V FOR SM
1) For children only: added “extreme clinging”
and not being able to speak in social
situations.”
2) Classified under “Anxiety Disorders.” No longer
under “Disorders first diagnosed in infancy,
childhood, or adolescence.
DIAGNOSTIC FEATURES
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
Children will speak in their home or in front of
immediate family, but not to close friends or
relatives.
Children with selective mutism often refuse to
speak at school, leading to academic or
educational impairment, as teachers often
find it difficult to assess skills such as
reading.

Will often communicate non-verbally.

May excel in non-verbal areas of school.
ASSOCIATED FEATURES OF SM
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Excessive shyness, fear of social embarrassment, social
isolation and withdrawal (Carbone et al. 2010; Cohan et al. 2008)
Clinging, compulsive traits, negativism, temper
tantrums, or mild oppositional behavior (Cohan et al., 2008)
Almost always given an additional diagnosis of another
anxiety disorder—most commonly, social anxiety
disorder (social phobia) (Viana et al. 2009)
DIFFERENTIAL DIAGNOSES
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Communication disorders
Neuropsychiatric disorders/Schizophrenia/
Psychotic Disorders.
Social Anxiety Disorder (Social Phobia)
PREVALENCE/AGE OF ONSET OF SM

Relatively rare. 0.03 - 1%

2.7 – 6.8 yrs. (Cunningham et al., 2004)

(Bergman, 2002, Viana et al., 2009, Carbone et al., 2010)
Does not vary by race, sex, or ethnicity. More prevalent in
children vs. adolescents or adults.

Usually unrecognized until child enters school.

Usually not disruptive so it can go unrecognized.

Cultural issues- language barriers.

Duration: Unknown. Many grow out of it but retain features
of anxiety disorders throughout lifetime.
RATES OF COMORBIDITIES FOR SM
1. Other anxiety disorders (60-97%)
(Kristensen, 2001)
- SAD (44-100%; odds 1.6-8) (Anstendig,1999; Vecchio and Kearney, 2005; Arie et al., 2006; Manassis et
al. 2007)
- Avoidant personality disorder (17-30%) (Chavira et al., 2007)
- SAD, avoidant disorder, or both (97%) (Black & Uhde, 1992)
- Separation Anxiety (17-31.5%) (Black & Uhde, 1992; Kristensen, 2000)
- Specific Phobia (30-50%) (Manassis et al., 2003)
2. Externalizing disorders
- ADHD (11.1%) (Arie et al., 2006)
- ODD (6.8%) (Manassis et al., 2007)
3. Other disorders
- Enuresis (17-30%) (Black and Uhde, 1995; Kristensen 2000)
- Encopresis and tic disorder (7%) (Kristensen 2000)
- Phonological disorder (40%) (Kristensen 2000)
-Other language disorder (11.5-17.3) (Kristensen 2000)
SM, AN EXTREME VARIANT OF SAD?
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Children with SM compared to children with another
anxiety disorder are generally rated the same on
internalizing measures, general anxiety, and social
anxiety. (Vecchio and Kearney, 2005)
Age of onset is usually younger
SAD kids have higher reported anxiety levels, but the
differences are most likely a result of behavioral
avoidance leading to underreporting of symptoms in SM
kids (Kristensen, 2001; Melfsen et al, 2006; Viana et al., 2009)
SM may be more akin to severe avoidance behavior.
SM kids most likely have anxiety. It may not matter how to
categorize because they respond equally to similar therapy/
Tx.
EVIDENCE FOR SM AS AN ANXIETY
DISORDER



Determining etiology is difficult (biased parental
report, teacher, etc.) regarding core fear.
Large studies are difficult to do given the rarity.
Few objective data that determine the presence of
emotional arousal
Scott and Beidel, 2011
EVIDENCE FOR SM AS AN ANXIETY
DISORDER


Children with SM report similar levels of anxiety as
children with SP (Yeganeh et al., 2006)
Emotional Regulation Theory
Intensity, duration, and expression of anxiety dysfunctional
 Becoming selectively mute is a developmental mechanism
employed in order to avoid extreme emotional arousal

ETIOLOGY OF SM

Genetic
Concordance rates = Mothers (18%); Fathers (9%);
Siblings (18%) (Remschmidt et al., 2001)
 Parents more often than controls have Social anxiety
and “shyness” (Remschmidt et al., 2001)
 Mothers more often have other psychopathology
(personality disorders, avoidance, shyness, withdrawal)

(Chavira et al., 2007)

Family Dysfunction/Poor Reinforcement Strategy
Creates an environment that promotes dysfunction
 Model anxious behavior/limit social interaction
 Reinforce avoidance behavior


Behavioral Inhibition
COMMUNICATION DISORDER SM

SM typically do worse on nonverbal
communication tests than SAD kids
(Manassis et al., 2003)

Difficult to ascertain due to temporal issues
May be mute due to language difficulties
 Also, the muteness may develop into language difficulties


Similarly dysfunctional to SAD kids in social
skills, communication skills, and classroom
achievement (Carbone et al., 2010)
TRAJECTORY FOR SM


Most grow out of it.
Almost all transfer some of the maladaptive
social skills into adolescents and adulthood
(Joseph et al., 1999; Remschmidt et al., 2001)

The more the behavior is reinforced, the more
rigid and resilient it becomes. Most likely an
active way to decrease arousal, but shouldn’t
be considered oppositional (Scott and Beidel 2011)
The END
REFERENCES
SUPPLEMENTAL
COMPARISON OF THERAPIES

CBT vs. Psychodynamic; Bogels et al., 2014.



Both therapies showed clinically significant improvements
as shown by reliable change index.
Posttest = 64% of CBT and 63% of PDT; 3 mo. = 58%, 50%
No longer meeting diagnostic criteria, scoring below SPAI
cutoff. Still, social validity should be evaluated.
Amygdala
Hypothalamus
Pituitary/Adre
nal
Reticular
activating
system
Cortisol
Norepinephrine
Pupil dilation, heart rate,
muscle constriction
BAD ASS NEW MODEL
HERITABILITY

OF
BI
Robinson, Resnick, Kagan, Corley, 1992
A NEW MODEL

Essex et al., 2010

Takes into account maternal stress and gender
SOCIAL COGNITION MODEL FOR SOCIAL
ANXIETY DISORDER
“I must always sound
Intelligent” leads patients
to appraise situations
as dangerous which
generates anxiety.
“The anxiety and
negative appraisal
are maintained in a
vicious cycle.” (Clark and McManus 2002)
