chap 2 - social anxiety (* = sidetones)

SAD criterion A to E

social anxiety disorder (SAD) as “marked fear or anxiety about one or more social situations in which the person is exposed to possible scrutiny by others” (criterion A)

that person with SAD “fears that they will act in a way or show anxiety symptoms that will be negatively evaluated (i.e. humiliating, embarrassing or lead to rejection) (criterion B) *imp of fear of negative evaluation in social anxiety

social situation almost always provoke fear or anxiety (criterion C) & that these situation are avoided/endured with great distress (criterion D) *50% of ppl with SAD experince panic attacks — those that experience panic attach have greater fear/avoidance of social situations

fear or anxiety is out of proportion to the actual threat posed by the social situaiton & to the sociocultural contect (criterion E)

*ppl with social anxiety have poor insight (ex. high schooler with SAD avoids cafeteria bc she is convinced that everyone is looking at her — lacks insight to realise that ppl are focused on their own food (& not her)

SAD criterion F to J

for SAD diagnosis, fear/anxiety must have lasted for 6 months or more (criterion F) — to rule our social anxiety due to life transition or normal child development

the fear/anxiety/avoidance must cause signifigant impairment in functioning (criterion G)

SAD cannot be diagnoses if the symptoms are better explained by use of a substance (criterion H), symptoms of another mental disorder (criterion I), or a medical condition (criterion J)

*BUT if anxiety symptoms are related to medical condition, a diagnosis of SAD may be given if they are clearly excessive (as judged by comparison to other person with the medical condition)

generalized subtype of social anxiety (fear of social situation) was removed from DSM-5 bc most ppl with social anxiety fear multiple social situations — DSM-5 now lists diff specifier is dianostic criteria for SAD (ex. performance only SAD assigned to ppl whose anxiety is limited to public speaking or performing in public)

social anxiety disorder VS social phobia

social phobia — name in earlier editions of the DSM but experts didn’t think it captured the impairing nature of this disorder

social anxiety disorder (SAD) — preferred name for the disorder in teh DSM-5

SAD liked to signifigant impariment in social, educational & occupational functioning AND brings substantial economic & social burden

*ppl with SAD less likely to be married, more likely to have fewer friends, etc.

earlier version of DSM VS DSM-5 (for SAD)

self-perpetuating interpersonal cycle (def) — Alden and taylor (2004)

the interpersonal difficulties experienced by the individuals with SAD

idea that socially anxious ppl go inot social interactions expecting negative evaluations & therefore behave in ways that “pull” on other ppl to evoke response that maintain social assumptions

3 ways socially anxious ppl 'exert this pull' 

1)Safety behaviours — ppl with SAD rely of dafety behaviours: actions perceived by a person as necessary to prevent the occurance of a feared outcome. BUT these safety behaviours often backfire *reinforcing feared outcome

ex. if person with SAD fears his voice will shake when he speak, he may speak very softly or not at all — BUT in doing so, he increasing the likelihood that he will sound off/more broadly ppl will not want to talk to him

2)Distance themselves emotionally from others — ppl with SAD distance themselves emotionally from others, engaging in less self-disclosure (than nonanxious ppl). W

3)Fear of ppl getting to know them — fear that if ppl “rlly got to know them” they woudl ultimately reject them due to insecure, fearful attachment patterns stemming from childhood. these ppl tend to be more dependant in their relationships (than those without SAD, & this dependency takes a toll on their signifigant others)

*note: ppl with SAD show signifigant impariment in the workplace, lower lvls of educational attainment, & reduced income/higher rated of unemployment

cultural differences in SAD

similar rates fo SAD btwn US and in South American countries BUT lower prevalence rates in Asian countries (less than 1% for 1 yr prevalence)

asian race/ethicnity associagted with low prevalece in US samples as well

In US samples, being hispanic or black is also assocaited with lower risk (compared to being non-hispanic white)

tahjin kyofusho (TKS)

TKS is variant of SAD prevalent in Japenese & Korean cultures (but can occur in US too)

those with TKS worry about embarassing another person (ex. person w/ TKS may be so concerned about embarasing others with his body for that he avoids most social situations)

if we screen for SAD in our typical ways, we might miss this unique but highly impairing disorder which may explain why rates of SAD are so low in Asian populations (imp of cultural considerations of the DSM criteria)

age of onset for SAD

ranges from 13 to 20 yrs old — BUT many patients recall having struggled all of their lives with shyness & fear of negative evaluation (ex. '“i can’t remember a time when I wasn’t anxious about social situations”

SAD is more common in women (than men)

gender differences emerge in adolescence — men take longer (than women) to seek treatment, but men slightly outnumber women in clinical samples

this discrepency is bc of cultural norms for social behaviour: costs of not pursuing treatment may be higher for men (as they are expected to be outgoing and assertive), while women it may be more acceptable to be shy & reticent

SAD & Axis 1

SAD is assocaited with a high level Axis 1 comorbifity

based on survey, ~66% of ppl with SAD also meet criteria for another psycholgical disorder

SAD often precedes the onset of comornbid conditions — this chronology suggests that SAD may be risk factor for the dev of other psychiatric disorders

comorbid depression & SAD treatment

mixed findings for whether comorbid depression negatively affects the outcome of treatment for SAD — some studies suggest that ppl with comorbid depression make as much improvement during treatmetn as patients without depression but 2 studies did end treatment with more SAD symptoms bc they began treatment with more sever symptoms

other studies how high lvl of depressive symptoms are associated with poorer outcomes & high lvls of attrition (droppping out) — pattern of depression interfering wih SAD treatment

long-term maintenance of gains in ppl with SAD & comorbid depression — although patients w/ comorbid depression did just as well as patients wihtout depression during acute tratment for SAD, depression was aossociated with poorer amintance of gains one year later

disorders that most frequently co-occur with SAD

SAD most frequently co-occurs with other anxiety disorders (*GAD)

MDD is also very common in ppl with SAD — over 1/3 of ppl diagnosed with SAD report having experienced a major depressive episode at some time in their lives

*also alcohol use disorder, avoidant persoanlity disorder (ADP), & cannabis use

ppl with BOTH SAD and depression have an earlier age of onset of their depression, greater # of depressive episodes, longer episodes & more suicidal ideation (compares to ppl with only depression, no SAD)

this co-occurence fo SAD & depression also associated with greater impairment than either disorder alone (— less likely to marry, go to college & have stable employment)

relationship btwn SAD treatment & depression improvement (mediation & limitations — study)

unclear whether depression decreases with succesdul treatement of SAD or whether depression specifc-interventons need to be added to treatment for this comorbidi group

Erwin et al., (2002) showed that lvls of depression were reduced by cognitive-behvaioural group thoeryapy for SAD

BUT when examined in depth with Moscovitch et al. (2005): improvement in depression (which was not the target of the treatment) was fully mediatred by improvement in social anxiety — patients’ moods improved (depression decreases/improved) bc their social anxiety improved

limiations to this study: small sample size, study not designed specifically for patients with SAD & comorbid depressions

comorbidity btwn SAD & alcohold use disorder

SAD frequently comorbid with alcohol use disorders especially (subtance use disorders)

~50% of ppl with lifetime diagnosis fo SAD alos meet criteria for lifetime diagnosis of alcohol use disorder

ppl with BOTH SAD & alcohol use disorder are more impaired than ppl with a a diagnosis of SAD alone (similarly to comorbid depression & SAD)

this is in pt bc of high rates of toher comorbidities that occur in this group — ppl w/ comorbid SAD & alcohold depedance has mean of 4.6 additional disorders (almost twice the # seen in ppl with either SAD or alcohol dependance — Schienier et al., (2010))

SAD as risk factor for alcohol dependence

onset of SAD typically precedes onset of alcohol dependance — suggesting that SAD is a risk factor for alcohol problems

—Ex. fear of scrutiny (i.e. fear of being observed by others) is unique pt of social anxiety that places ppl at risk for later dev of alcohol use disorders

other studies: alcohold use prior to speech reduced anxiety & blushing during speech, drinking associated with less post-event processing 4 days after convo w/ person of opposite sex, but only for socially anxious women

the few studies that administer alcohol proor to or during a socially stressful task reinforce effects of alcohodl use for sociallu anxious ppl

challenges & approaches to treating comorbid SAD and alcohol dependence

ppl w/ comorbid SAD & alcohol dependance report very low rates of treatment seeking

little research on how to best reat this group: most studies of treatment for SAD exclude ppl w/ substance use problems

one study (Kushner et al., 2013): ppl w/ SAD in residential alcohold treatment program — treatment with CBT designed to lower social anxiety & weaken links btwn social axniety and motivation to drink was assocairted with reduced drinking 4 months posttreatment

other study using CBT to lower SAD & substance use only lead to decrease in SAD but no change in alcohol use

proposal to combine motaivaional enhancement therapy for alcohol use disorder & CBT for SAD

canabis use in patients with SAD

SAD is more strongly related to cannabis dependance (than to cannabis abuse)

SAD typically comes before cannabis use & that ppl with this comorbidity experince greater impairment than ppl with either disorder alone (*again like comorbid depression & alcohold use disorder w/ SAD)

Ex. Tepe et al., (2012) study: ppl w/ comorbid SAD & cannabis use disorders are also more liley to haev lifetime diagnosis of PTSD, specific phobias & other substance ue disorders (that ppl with either disorder alone) — provides durther support to the impairment likely seen in this group

comorbity btwn SAD & avoidant personality disorder (APD)

SAD is highly comorbid with APD — median of 60% of ppl with generalized SAD (accordingto earlier versions of DSM) meeting criteria for APD

considerable overlap in criteria for these 2 disorders

APD def: “pervasive pattern of social inhibition, feelings of inadequacy, & hypersensitivity to negative evaluation, beginning by early adulthood, and present in a variety of contexts”

genetic & family studies suggest that SAD & APD are strongly related — BUT studies that have tried to find what differentiates the 2 disorders, find nothing clear

it has been proposed that APD may be assocated with greater persoanilty dysfunction (than SAD)

another description of relationship btwn SAD & APD — that they are not diff disorders and that instead, APD representes the most severly impaired persons w/ SAD

ppl w/ both SAD and APD tend to be more depression & have greater functional impairment & quality of live (compared to ppl with SAD alone)

genetics & SAD

genetics have imp role in dev of SAD

family studies show higher rates fo SAD in relatives (proband) of person with SAD (than in proband/raltives of person without the disorder) — suggests that SAD is moderately heritable

generalized SAD shows stronger familar aggreation (than non vernalized SAD)

twin studies support role of genetics in heritability of SAD & social anxiety-related symptoms (i.e. behavioural inhibition, fear of negative evaluation)

both twin studies & genetic linkage studies suggest that SAD & panic disordeer might share common susceptibility genes — these 2 disorders are often comorbid & share mnay clinical features

genetic influences on behavioural traits linked to SAD

due to complexity of psychiatric disorders — unlikely that a single gene or group of genes lead to the transmission of a specific anxiety disorder

instead reasearchers believe that “some underlying behaviours trait (i.e. behavioural inhibition or neuroticism) is thought to be genetically transmitted, contibuting to spectrums of psychopathology” * Traits Over Specificity

specific genetic variations have been found that are related to neuroticism, introversions/extraversion, behaviourally inhibitted temperment, shyness in childnre, & incrases activtsion of amydala & insula on exposure to emotional faces — all relavent to the pathology seen in SAD

4 brain regions implicated in SAD *PIAF

1)amydala (pt of brain’s fear pathway, forms & stores emotional memories): ppl w/ SAD showed greater actication of the amygdala in response to threatening faces, w/ greater magnitude of activation associated with severity of SAD

2)insula (interoceptive awareness — ability to be aware of internal sensations in the body, including heart rate, respiration, etc.): increased activity in insula when ppl with SAD are shown socially relevant stimuli (i.e. negative facial expression or social transgressions)

3)fusiform cortex (brain region associated with facial recognition): mixed findings — ppl w/ SAD shown increased activiation in this area, but other decreased activation when shown range of facial stimuli

4)prefrontal cortex (PFC — used for panning, problem sovling, social behvaiour & emotion regulation *the 2 later most relevant to SAD)

relationship btwn amygdala & PFC in SAD

same socially relevant stimuli that leads to activiate of amygdala also leads to activation of prefrontal cortex

— this suggests that once fear is acticated by the amygdala, ppl w/ SAD process this info in diff way than ppl without the disorder

in study, more effortful for ppl with SAD to reappriase negative self-beliefs (compared to healthy controls

link bvtwn fusiform cortex, SAD & Aspergher’s syndrome

hypoactivation of fusiform cortex seen in ppl with Asperger’s synrome; a disorder marked by poor social connectedness

ppl with SAD may hone in on social stimuli to gain support fo their negative beliefs (e.g. focusing on the person in the audiance who is dozing off during a presentation)

ppl with SAD may shift their attention away from faced (ex. averted eye contact)

so those mixed research findings may capture the complexities of SAD

3 neurotransmitters implicated in SAD

1)serotonin (SSRIs — selective serotonin reuptake inhibitors)

2)dopamine

3)oxytocin

serotonin & SAD

Serotonin has unclear role in SAD

BUT in studies, when ppl w/ SAD given agents that release/mimic serotonin, they experience an increase in anxiety

yet SSRIs (which make available greater lvls of serotonin in synaptic cleft) have been shown to reduce anxiety in other studies

one explanation for inconsistency in studies: increased lvls of serotonin may have diff short-term VS long-term effects — this is supported by clinical studies when patients start taking SSRIS, they often expense an initial icnrease in anxiety, followed by improvement in their anxiety symptoms

dopamine & SAD (4 pieces of evidence of links)

1)monoamine oxide inhibitors (which work on both dopaminergic & serotonin systems) are effective in the treatment fo SAD, while tricyclic antidepressants (which work on serotonin & norepineprhine systems) are NOT — show efficacy of dopamine

2)low dopamine transporter density had been found in ppl with SAD

3)higher than expected rates of SAD are seen in ppl w/ parkinson’s disease — drugs used to treat parkinson’s facilitate dopamine transmission (so ppl w/ parkinson’s have low dopamine, low dopamine couls bve linkd to SAD)

4)low dopamine receptor binding potential in striatum region of brain also been found in ppl with SAD — same deficit found in animals w/ subordinate status, which ahve been used as model for human SAD

oxytocin & SAD

oxytocin is a neuropeptide associated w/ social appraoch behaviour & bonding

research suggest that impariments in oxytocin system may play role in SAD (as well as other disorders characterized by deficits in formation of social bonds (i.e. ASD, postpartum depression))

possible that oxytocin could serve as novel treatment or supplement to more commonly used treatments for SAD

cognitive-behavioural models of maintenance (CBM) of SAD

they have been proposed to explain the self-sustaining nature (maintenance) of SAD

according to these models, beliefs that social situation are inhernetly dangerous & that ppl are inehertnly criical, along with behvaioural avoidance & phyciolligcal symptoms, are crucial structures that maintain social anxiety

2 main theories: Rapee & Heimberg (1997) AND Clark & Wells (1995)

core feature of SAD

dev & maintenance of social anxiety is accounted for/by fear & negative imagery of self and others

core feature of SAD is described as fear of any evaluation, either negative or postive (not only negative like traditionally thought!)

fear of evaluation develops out of beliefs that social/performance situations are dangerous & that other ppl are critical (of you)

Rapee & Heimberg (1997) CBM model (4 pts?)

1)upon entering a social/performance situation, person w/ SAD allocates theirs attention 1st to audiance, and by using certain cogtnive biases, they result in the prediction that they will fall short of the perceived standard of the audiance

2)then, a person w/ SAD creates a mental representation of the self as seen by others, engaing in negative self-imagery such that their self-image is from this presumed critical observer’s perspective

3)info taken from person w/ SAD’s first impression of the audiance’s reaction is combined w/ info from past similar situation as well as internal AND external cues (ex. heart palpiations, ppl’s ‘look of distaste’) to make assessment of how the audience is likely to view them — person w/ SAD constantly monitors their behaviour & behaviour of others to determine

4)BUT ironically, attending to both these multiple factors & social/performance at hand may increase the probabilty of poor performance — evidence confirming their poor performance will be weighted more heavily than evidence to teh contrary (for ppl with SAD)

post-event processing (PEP)

confirmatory evidence of neagtive evaluation is likely projected to future catastrophic outcomes (ex. social rejection, extreme lonliness, etc.)

these negative thoughts provide the content for post-event processing (PEP): the biased, distorted & ruminative cogntive process that contributes consistenlty to the maintenance of SAD & that links one occurance of a fear social situation to the next

evolutionary theories of etiology of SAD & fear of postive evaluation

*similarly when person w/ SAD performs well, they are likely to avoid similar subsequent situation bc they believe that they will have to meet similar or evn increasingly postive expectations (fear of postive evaluation)

3) (person w/ SAD constantly monitors their behaviour & behaviour of others to determine) is consisent with evolutionary theories of etiology of SAD

person w/ SAD hypothesized to both avoid drawing attention to themselves & to work to maintain low soical status so that they can avoid etiher losing or having to engage in conflict in other to defend higher social status,

this is consistent with notion of fear of postive evaluation

Clark & Wells (1995) (VS Rapee & Heimberg (1997) CBM model of SAD)

propose that attention of the person with SAD is largely focused on internal symptoms of anxiety, which are then used to support the belief that others are indeed evaluating them negatively

they also suggest that subtle avoidance behaviours (ex. conversing but remaining passive in the convo) play a central role in the maintenance of SAD

propose a similar internal focus of attention (to Clark & Wells, 1995) BUT further assert that the negative attention of the person with SAD is split btwn this internal focus & an external search for indicators of this evaluation

maintain that all unhelpful anxiety management strategies (ranging from subtle to complete avoidance) all contribute to the maintenance of a disorder

attentional bias (def & two types)

def: idea that ppl attend preferentially attend to info in the enviro that they find particularly relevant (ex. when engaged in public speaking, a person w/ SAD tends to notice one bored looking person VS the 99 others who appear interested in presentation)

2 types for anxiety: 1)orienting biases toward threat (or hyperviglience for detecting threats) OR 2)difficulty disengaging attention from threat (or difficulty shifting attention away from threat once attention has been captured)

for both hypothesized that paying attention to social-threat-relevant info (instead of more neutral or postive social info) makes the person more prone to anxiety

emotional stroop paradigm

emotional stroop paradigm: participants are first showed socially threatening & neutral words printed in various colours

then asked to respond by naming the colour as fast as possible (instead of reading the word)

slowed responses (to naming the colour) suggests that the content of the word has captured participants’ attention, making it more diffcult to quickly report the colour

dot-probe paradigm

dot-probe paradigm: participants are showed 2 stimuli (ex. words or faces), one neutral & one emotionally valenced

these stimuli are presented briefly follow by a dot (or other probe stimulus) in place of the stimuli

if participants respond faster to the probe displayed in the same location as the emotinally valence stimlus (compared to location of neutral stimuli):

participants may be attending preferentially to that emotionally-valanced stimlus instead of looking away from it or focusingon the neutral stimlus

limitations of emotional stroop & dot-probe paradigm

emotional stroop: slowed colour naming of socual threat could instead show biased attention or cogntive avoidance

dot-probe paradigm findings have been criticized for inconsistent findings, attentional bias toward threat being uncommon in ppl w/ SAD & the dot-probe’s poor psychometric properties

— inconsistent findings ex. early studies using dot-probe supported attentional bias toward threat: ppl w/ SAD faster (than controls) to identify prob when it appeared in the same location as the threat stimlus (compared to appearing in saem location as neutral stimlus)

but recent suites have seen biased attention away from threat: faster responses to probes follwing netural stimlus (instead o social threat stimlus or null results)

fine-tuning conceptualization & assements of attentional bias

in response to complex findings of whether attentional bias has causal effect on anxiety — can we can traint ppl to attent to neutral rater than threat info and if this can help alleviate this anxiety?

1)one way they have done this is by looking at “attentional bias toward threat”: studies show that ppl with higher anxiety often struggle with deliberatre or efforful control of attention. These findings are backed by tasks that are scientifically reliable — psychometrially sound

2)another way is that researchers have considered that degree & type of threat-realted attentional bias may vary considerably btwn VS within ppl w/ SAD — ppl w/ SAD who showed general pretreatment attentional bias away from threat did worse in CBT (than those that showed a bias toward threat)

— this suggest that attentional bias is NOT UNIFORM across ppl with SAD & supports finding that traditional SAD CBM-A (cog bias modification of attention, which trains attentinoa away from threat) may ONLY be effective of ppl with SAD who show bias toward threat

*attention may vary within same person over time: ex. attnetional bias in ppl w/ spider phobia has been found to be dynamic (not static) during dot-probe task

2 effects of SAD on social interactions & relationships

1)ppl with SAD go into social interaction looking for cues that support expectation that they will be evaluated — such hypervigilence for threat may lead socially anxious person to notice relatively harmless cues (ex. interactin partner may furrow his brow during brief moment of disagreement, & while this cue may go unoticed by most, for person w/ SAD who is apt to notice it, they will percive it as they’re acting in a socially unacceptable manner)

2)avoiding threat info or having difficulty controlling attention (i.e. missing social postive cues) can negatively affect social interactions (in new and established relationships)

— ex. if s/o looks away forn convo partner, she may miss on on imp social cue that would make the convo flow well (ex. postive cue like other person' smiling, nodding, etc. that would show person w/ SAD that they are doing well in interaction)

— ex. in established relationsups, poor eye contact may make non-axious friend feel like friend w/ SAD is not being open or honest so this simple protective stance can put strain on quality of both new & estblished relationships

judgement & interpretation bias

1)socially anxious ppl tend to be their own worst critics — socially anxious ppl & those w/ SAD judge themselves more negatively (than they judge others) AND judge themselves more negative (than they are judged by others)

—bc socially ancious ppl judge themselves so harshly, it’s not suprising that they enter social situation assuming that others will do the same

2)ppl w/ sad are more likely (than controls) to assume that other ppl interpret physical symptoms they show (ex. blushing, sweating, etc.) as signs of an intense anxiety problems or some other psychiatric disorder (rather than some benign explanation like being too hot)

4 characteristics of interpretation bias in ppl w/ SAD

ppl w/ SAD overestimate the prob of negative outcomes in social situations & greatly overestimate the cost of these outcomes

ppl w/ SAD tend to interpret both ambiguous social events & mildly negative social events as extremley negative & catastrophic

ppl w/ SAD tend to negatively interpret social info & fail to accept others’ postive reactions as face value

when interpretation bias is inferred from relativley automatic process (ex. event-reated brain potentials) socially anxious ppl also appear to lack the postive or nonthreat interpretation bias (that is typical in nonanxious individuals)

CBM-I & its effects on social anxiety

cogntive bias medications of interpretations (CBM-I) used to see whether interpreations biases cause anxiety

repeated trainging to make benign (harmless) interpreations of ambiguous scenarios has resulted in reduced threat interpreations & reduced social anxiety in ppl w/ high social anxiety

recently as internet-based application of CBM-I has shown potential to reduce threat interpretations & anxiety symptoms in ppl w/ SAD

ex. study: a control CBM-I condition was as efficient as the active condition in reducin anxiety (but not interpretation bias) in a an internet-based stay in a mixed anxiety sample

socially anxious ppl, the situations they put themselves in and the judgmens they male

research on judgment and interpretation bias suggests that socially anxious ppl routinely put themselves into no-win situations — any socially relevant info (negative, ambiguous or postive) is percieved negative & intepreted as costly, which affects quality of social (why socially anxious ppl are compelled to avoid social situations)

based on lab studies (asking ppl what kind of judgment they would make if certain experiences happen to them e.g. seeing a table of ppl laughing as you walk by), socially anxious ppl assume that they would make negative & costly judgements in these hypothetical situations

ppl w/ SAD have a difficult time w/ self-disclosure & they often express fear that ppl would reject them if they really got to know them

explicit vs. implicit recall memory bias in SAD

research on memory bias focuses on whether socially anxious ppl preferentially remmeber socially threatenting indo relative to neutral info or info that is treatetning but lacking in personal salience

in general, studies in memoru bias have been inconsistent — most show no evidence of preferential recall or recgonition of social threat in ppl w/ SAD

an explicit bias is more likely observed when the encoding stimlus have personal relevance — study: when asked to rate faces as critical or accepting, ppl w/ SAD then recognized more critical than accepting faces (while opposite was true for controls)

but an implicit memory of retrieval (or retrieval of info that is leared as an unintended effect of experience & is tested indirectly) have revealed no evidence of a bias for social threat into

autobiographical bias: objective VS subjective aspects

it’s been suggest that ppl w/ SAD may preferentailly remember autobiographic social events but studies have been inconsistent — few studies w/ objective meaures (ex. # of memeories recalled) have found evidence of a bias

one exception study: Wenzel & Cochran (2006) found that richer retrieval cues (*negative cognitions related to social anxiety) resulted in retrieval of more anxiety-related memories & faster retrieval of these memories for ppl w/ SAD (comapred to nonanxious ppl)

BUT subjective aspects of memory (ex. associated emotions or memory content) have largely supported an autobiohraphical memory bias

Ex. ppl w/ SAD responded to memories of stressful social events w/ symptoms of hyperaroudal & avoidance (while controls did not, Erwin et al., 2006), ppl high in social anxiety recalled more negative & socual anxiety-related memories (than ppl low in social anxiety) when cued by emotion words & asked to recall “self defining memories”

—suggests that rich, personally relevant cues & assements of subjective content of memories are necessary preconditions for observing autobiographical memory bias threat in social anxiety

involuntary memory & visual memories in ppl w/ SAD

aka memories of personal evetns that come to mind with no preceding attempt at retrieval

in studies of mental imagery & visual memories, generally ppl w/ SAD experince repetitive, intrusive, negative & biased visual memories of themselves in social situations

Hackman et al., (1998): when patients asked to recall a recent social situion in which they delt anxious & to describe the image tha they had of themselves during it, ppl w/ SAD were more likely to report having a clear, negative self imagine that felt like a very accurate depiction of how they were coming acorss duign that event (compared to controls)

Hackman et al., (2000): when patients asked if they assocaited this negative self-image with a particular event, most could recall a specific past event in which they felt embarrassed & humiliated with this image clearly connected to the most negative aspects of this recalled event

autobiographical memories and social anxiety: links to ptsd-like distress

in Hackman et al., (2000) study, falls in line with the study by Erwin et al. (2006) on autobiographical memories in SAD

in that study, majority of patients w/ SAD recalled having experinced a socially stressul life event (like feeling humiliated after a poor public perforce or being rejecrted by a potential romantic interest)

these memories were accompanied by such significant symptoms of avoidance & hyperarousal that patients would have met criteria for PTSD had these events qualified as PTSD Criterion A events (so in other words, white the amount of distress)

it’s likely that patients in this study had negative self-images related to these soically stressful life events, just as pateints in the studies conducyed by Hackman et al., (2000) did

2 types of imagery perspectivesn & socially anxious VS not socially anxious ppl

1)field perspective: when ppl recall situation as viewed through their own eyes —ppl without SAD tend to take the field perspectivem

2)observer perspective: when ppl see themselves through the eyes of tohers (as if they are viewing themselves on videotape) — socially anxious people tend to recall social situations from an observer's perspective, imagining how others viewed them rather than focusing on what actually happened.

this perspective is often negatively biased, as they assume they know what others are thinking about them.

this belief causes them to remember themselves in an overly critical light & such negative recollections reduce their willingness to engage in similar social situations in the future.

negative self-imagery & maintenance of social anxiety

there is support for the idea that negative self-imagery contributes causally to the maintenance of social anxiety

in studies, participants have been trained to hold either a negative ro behign self-image in mind while engaging in a social task, negative self-imagery elicited higher self-reported anxiety in ppl w/ SAD, ppl w/ high social anxiety & event nonanxous ppl

systemic review: effects of negative self-imagery on anxiety were similarly harmful across the social anxiety spectrum SO there is greater prevalence of negative self-imagery among socially anxious ppl that contributed to the maintenance of anxiety

socially anxious ppl appear to spontaneously regulate negative self-imagery in maladxaltpve ways (ex. thought suppression) VS low anxiety ppl tend to make use more adaptive strategies (ex. altering content of their images)

interconnected cognitive biases in social anxiety

Hirsh et al., (200^): diff kinds of cogntiive biases interact with one another (better stood in that way together than in isolation)

research supports effects of negative imagery on interpretation biases, interpretation biases on memory biases, & interpretation biases on attnetion biases

ex. Jenkins et al., 2006 study: socially anxious participants were faster to retreive negative autobiographic memories when they held a negative self-image in mind

—participants in negative interpretation bias induction condition also produced more negative self-related images

5 parent/child influences in SAD

Ollendick & Benoit (2012): SAD originates from a “delicate interplay of parent & child influences”

they suggest 5 factors are imp to consider:

1)tempermental characteristics 2)Parental anxiety 3)Attachment processes 4Info processing biases & 5)Parenting practices

behavioral inhibition temperment

temperment that had been most studied for anxiety is the highly reacgive or “behaviourally inhibited” temperment

behvaioural inhibition is the tempermental tendency to display restaint, fearfulness or withdrawal when faced with unfamilar people, situation and objects

research suggests that behvaiourally inhibited temperament is a specific risk factor for SAD

BUT only ¼ to 1/3 of behaviourally inhibited kids develop SAD — suggests the interplay of other factors in the dev of SAD

parental anxiety

parental anxiety plays an imp role in SAD in children

children have been found to be at increased risk of developing anxiety disorder & SAD in paritucular, when their parents are anxious or when their parents have clinically signifigant panic disorder with agorophobia or SAD

this supports studies that show socially anxious children tend to grow up in homes w/ low lvls of family sociability

growing up with extremely shy parents can 3 main consequences

4 consequences of growing up with socially anxious parents

1)while growing up kids do not see their parents participating in strong, postive interpersonal relationships of their own

2)these children also also see their parents reacting anxiously in a variety of social situations

3)children of socially anxious mothers may learn about & imitate social anxiety from a young age

ex. in study where mother & her 10-month old baby had interaction w/ stranger, mother w/ SAD showed more anxiety & were less encourarging fo their baby’s interactions w/ the stranger (than nonanxious mothers/mothers without SAD)

4)in older kids, shy parents are less likley to faciltate peer interactions for their children — during kids’ early yrs, parents are involved in both planning playdates w/ other paretns + socializing during these playdates

Bogels et al. (2001) found children w/ higher lvls of social anxiety often have parents, especially mothers, who also experience social anxiety — these mothers tend to be more involved in their children’s daily lives.

By the time these children reach adolescence and start becoming more socially independent, they may struggle with social interactions. This is because the usual challenges of adolescence, combined with a lack of social experience, make these situations even harder for them.

role of early attachment to parents

proposed that ppl develop schemas for understanding theri social world via these earliest interpersonal relationships

quality of these relationships is thought to affect personality dev & quality of relationships later in life

securely attached children have parents who are attentive & responsive

insecurely attached childnren have parents who are rejecting & undependable — shyness & social anxiety during childhood are related to insecure attachment patterns during infancy (ex. shy adults tend to report having had paretns who were rejecting & lacking warmth)

—relationships have been found btwn SAD in adulthood & insecure attachment patterns

bidirectional relationship between social anxiety and peer victimization — McCabe et al., (2003)

relationship btwn social anxiety & peer victimization (ex. teasing) is bidirectional — peer victimization was both a predictor and a consequence of social anxiety

McCabe et al., (2003): recalled childhood teaching was much more strongly associated to adukt SAD (than to adult OCD or panic disorder)

AND higher frequency of recalled childhood teasing was associated w/ greater severity of adult social anxiety symptoms

impact of recalled social teasing on adult psychological distress and relationships

recalled teasing in the social domain (ex. being teased about looking shy/nervous) was more strongly related to psychological distress during adulthood (than recalled eashing in other domains)

recalled childhood teasing related to greater early adulthood impairment in interpersonal functioning — specifically less comfort w/ intimacy/closeness, less abilty to trust/depend on others, & greater degree of worry about ebing unloved or abandoned in relationships

emotional maltreatment found in childhood victimization may lead to dev of a negative inferential style, interpersonal deficits & hopelessness regardling one’s ability to change negative events

mixed findings for effect of parenting style on dev of SAD in children

parenting style plays imp role in dev of sad — but research findings mixed

found that SAD asociated w/ controlling, overprotective & critical parenting

But also found that parents who are warm/accomodating exacerbate avoidant behaviour in their (behaviorally) inhibited children

—possible that both these extremes of parenting (too much accommodation/warmth VS too much criticism/lasck of help) are poor fits of children at risk for SAD

traits of fam members w/ SAD in clinical practice

children & teens described as behaviourally inhibited since infancy (having SAD?)

parents recall them bein nervous around new ppl but also reactive to new toys, foods & routines

in fams: at least one parent describes themsleve as introverted, often only doing things withing nuclear/extended fam

tho parents of socially anxious kids tend to want to protect them from feeling anxious, they may also get angry/critivise theri kids for looking to anxious (which triggers parents’ own concern about negative eval for other (their SAD?))

if parents go to avoid anxiety, they facilate avoidance situations for their kids, kids never learn to cope w/ anxiety nor that their anxiety with lessen w/ repeated exposure to a feared situation — never seeing pleasent/rewarding social interactions, increases likelihood of continued avoidance into adolsecence & adulthood

semistructured interviews

these interviews are used to establish diagnoses + rate the severity of diagnoses (sometimes)

assessor is presented w/ a set of question to guide decision abotu presence or absence of DSM diagnosis, but also allows assessor flexibility to gain clear understanding of patient’s primary covers

this interview can greatly reduce the rates of false neagtives in diagnosis of SAD

3 most commonly used scales for anxiety disorder research setting

1)structured clinical interview for DSM-5-TR Axis 1 disorders-patient edition (SCID-1/P)

2)more recent DSM-5 research version (SCID-5-RV)

3)most recent Anxiety and Related Disorders Intevew Schedule for DSM-5 (ADIS)

pros & cons of SCID

pros: can be completed in a relatively bried & efficent manner

includes screening questions for each diagnosis that allows clinicians to skip sections that do not seem relevant to given patent & to skip cetainsection once they’ve made sure that criteria for given disorder are not met

cons: doesn’t cue clinicians to agther additional info on patient’s difficulties beyong DSM criteria — such data data may reduce false negatives

SCID is not sufficiently detailed to be used for treatment planning

pros & con of ADIS

pros: it includes numerous questions that go beyong DSM criteria, items that asks about triggers of anxiety (ex. feared social/performance situations) & reactions to these triggers (ex. avoidance/experience of situationally cued panic attacks)

questions are also asked about specific behvaiours, thoughts & scope of acoidance, & past history of social anxiety symptoms

this additional questions make the ADIS lengthly to administer (con), but provides valuable info for treatment planning

ADIS also allows clinicna to assign a clinical severity rating (CSR) for each diagnosis

clinical severity ratings (CSR)

CSR useful in both research & clinical settings

this rating of symptom severity allows for treatment planning, provides an estimate fo treatment length, and allows for assement of improvement over the course of treatment

Lisbowitz Social Anxiety Scale (LSAS)

it has 24 items: 11 about sotial interaction situations (ex. meeting strangers) and 13 about performance situations (ex. making presenations to a small group)

each item is rated according to the degree t0 which the patient has feared & avoided specific situation over the past week

LSAS is unique bc it assess specific situations (comapred to tohers measures that assess symptomalogy — prevalence of symptoms)

LSAS has strong validity, adequate discrimiant validity & is sensitive to treatment change — it’s also highly reliable

it’s a strong clinical tool — it can be used for both treatment planning & to assess improved ofer course of treatment (as it gathers info on diff social/perforamnce situation that patients fear and avoid — ex. creating hierraryching of fear situations)

most common self-report measures for social anxiety symptoms (in adults)

1)SIAS — social interaction anxiety scale

2)SPS — social phobia scale

3)BFNE — brief fear of negative evaluation

4)SPIN — social phobia inventory

5) SPAI — social phobia & anxiety inventory

SIAS & SPS

SIAS (social interaction anxiety scale) — measures ancety in dyads & groups

SPS (social phobia scale) — measures anxiety in situations in whcih the person may be criticaly observed by others

both have been shown be reliable for measuring SAD and valid

BFNE

brief fear of negative evaluation (scale)

12 item scale, assess core concern of ppl with social anxiety — fear of negative evaluation

more valid when only 8 straightforwardly worded item are used

strong psychometic properties

SPIN

social phobia inventory (SPIN)

17-item, assess 3 theoretical pts of social anxiety: subjective fear, avoidance behvaiour & physciological symptoms

good reliability & ability to distinguish btwn ppl w/ SAD VS other anxiety disorders

SPAI

SPAI (social phobia & anxiety inventory): asks about somatic, cogntive, & behavioural responses to social & performance situations

also askes about situations that are commonly feared by ppl w/ panic disorder & agoraphobia

consists of 45 items but bc some require multipel response, ppl can answer a total of 109 items

has 3 sub scales: social phobia, agoraphobia, & derived difference (or total score)

is valid, has good reliatbilty, and good test-retest reliability and is sensitve to treatment change