WEEK 6: Social anxiety disorder
1. Craske (2015): Optimizing Exposure Therapy for Anxiety Disorders: An Inhibitory Learning
and Inhibitory Regulation Approach
Inhibitory learning is the process that leads to extinction, so extinction and inhibitory learning
aren’t two alternative explanations. ILM is a model of how to achieve extinction of the CS-US
association.
Exposure therapy refers to repeated, systematic exposure to cues that are feared, avoided, or
endured with dread.
o imaginal
o in-vivo to actual objects
o interoceptive to bodily sensations
Exposure therapy is highly effective alone or in combination with cognitive restructuring or
somatic strategies.
However, it is not effective for everyone.
o 25-30% refuse to begin exposure therapy
o 15-30% fail to complete treatment
o 50% fail to achieve clinically significant improvement
o 19–62% demonstrate a return of fear after treatment
Mechanisms of exposure therapy: Inhibitory Model of Extinction
Habituation theory: provides a descriptive framework for responses during exposure therapy
because self-reported fear and physiological arousal most often decline within and across exposure
occasions, but support for the theory has been inconsistent. Evidence shows the amount by which
fear declines from the beginning to end of an exposure session does not significantly predict self-
report questionnaires or behavioral avoidance testing at follow-up.
Inhibitory learning is central to extinction: the original CS-US association learned during threat
conditioning is not erased during extinction, but rather is left intact as a new, secondary inhibitory
learning about the CS-US develops. After extinction, the CS possesses 2 meanings; its original
excitatory meaning (CS-US) as well as an additional inhibitory meaning (CS-noUS).
Retention of at least part of the original association can be uncovered by various procedures:
1. when a lot of time has passed since extinction training
2. when the context between extinction and retest has changed
3. if unsignaled US presentations occur between extinction and retest
4. if the CS-US pairings are repeated following extinction
Clinical translation of the inhibitory extinction model to exposure therapy:
1. An individual enters treatment with a threat expectancy.
2. As a result of exposure therapy, a competing non-threat expectancy develops.
3. After completion of exposure therapy, the level of fear that is experienced when the
stimulus is re-encountered is dependent upon which expectancy is activated.
a) Activation of the original threat expectancy will enhance the expression of fear (if a lot
of time has passed since completion of exposure therapy; if exposure is done in a
limited number of context; if exposure is not practiced after training)
, b) whereas activation of the exposure-based non-threat expectancy will lessen fear
expression.
The level of fear expressed during or at the end of exposure therapy has no relationship to
the factors responsible for which expectancy is activated.
Deficits in inhibition in anxiety disorders
Individuals with anxiety disorders show deficits in EXTINCTION learning and related
mechanisms they exhibit stronger responding to the CS+ during both conditioning and
extinction. Hence, they show:
1. weakened extinction (elevated responding to CS+ during extinction training)
2. long term deficits in extinction (elevated responding to the CS+ at extinction retest)
3. elevated responding to the CS–
One explanation: individuals with anxiety disorders show impaired INHIBITORY learning.
o Central to the pathology of anxiety disorders is impaired inhibitory (or safety) learning to:
a) either a stimulus that does not signal threat (CS–)
b) or to a stimulus that no longer signals threat (CS+ during extinction)
Individuals with, or at risk for, anxiety disorders appear to have difficulty inhibiting their
fear to specific cues that should represent safety when they occur within a threatening context.
Evidence for impaired inhibitory mechanisms has been established for PTSD, highly
traumatized samples, and those with greater state anxiety.
Extinction is mediated by inhibitory learning/regulation and individuals with anxiety disorders
possess deficits in such inhibitory learning/regulation, which may serve as a risk factor for
anxiety disorders.
Optimizing exposure strategies
These strategies are derived from principles of fear extinction and inhibitory regulation.
Violation of expectancies
o Exposures are designed so that the experience maximally violates the negative, excitatory
expectancies regarding the rate or frequency with which aversive outcomes occur, which
should enhance the development of inhibitory, non-threat expectancies.
o The greater the mismatch between what is expected to occur and what actually occurs, the
greater the opportunity for learning.
o Exposure trials can disconfirm expectancies regarding the temporal latency, frequency, and
intensity of negative outcomes.
o It is first established what the individual is most worried about (i.e. threat expectancy), and
then design the exposure to disconfirm their expectancy.
o Deepened extinction
When multiple fear conditional stimuli are first extinguished separately before being
combined during extinction.
, Such strategies reduce spontaneous recovery.
For example, exposure to one specific type of spider, then a second distinctly different
spider, followed by exposure to both spiders at the same time.
The goal is to learn (explicitly or implicitly) that the aversive event occurs less often or is
less intense than expected.
o Occasional reinforced extinction
Involves occasional CS-US pairings during extinction training (occasional social rejection,
panic attack etc.).
Reduces rapid reacquisition effects.
The benefits may derive from an expectancy violation effect.
Even though occasional reinforced extinction sustains fear arousal during extinction, it
attenuates
the subsequent reacquisition of fear.
o Cognitive restructuring strategies
Cognitive strategies may be helpful in generalizing extinction learning to additional
stimuli, which can be beneficial because extinction is usually very stimulus-specific.
May help mitigate conditioned fear responding through reinterpretation of the
intensity of the US so the person is more likely to engage in exposure.
However, they can also negatively impact exposure by reducing US expectancies prior to
exposure, mitigating extinction learning.
Stimulus variability
o Varying the to-be-learned task enhances retention of learned non-emotional material, because
it enhances storage capacity of newly learned information.
o Variable stimuli resulted in less fear at follow-up.
o We routinely conduct exposure with varying stimuli, for varying durations, at varying levels
of intensity.
o Such variability typically elicits higher levels of physiological arousal and subjective anxiety
(as opposed to habituation models in which fear is supposed to diminish already during
exposure).
o In variable exposure, exposure is conducted to items from the hierarchy in random order
(starting with the less anxiety-inducing one to prevent dropout).
Enhancing retrieval of inhibitory learning
o Consolidation scheduling
Progressively increasing periods of time between learning trials enhance the retrievability
of newly stored information.
Similarly, progressively increasing amount of time between exposure practices is more
effective at follow-up than massed exposure.
This speaks to the value of booster sessions following completion of exposure therapy.
o Retrieval cues
One option for enhancing retrieval of extinction is to include retrieval cues during
extinction training to be used in other contexts, once extinction is over, to remind them of
what they learned during exposure therapy.
One risk of retrieval cues, however, is that they may become a safety signal.
Hence, these strategies are best employed as a relapse prevention skill.
o Scopolamine
