Kim's Exam Question Exposure Therapy Flashcards
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
a) background for fear extinction and exposure therapy
Fear extinction underlies exposure therapy for anxiety disorders and PTSD. Development of anxiety disorders and PTSD is due to fear conditioning — the pairing of fear response with a US leads to a conditioned fear response when the CS is presented. Although a meta-analysis showed that anxiety and PTSD patients do not have greater conditionability, they have impaired fear extinction (i.e., greater arousal and reduced ventro-medial prefrontal cortex activity during extinction recall). Hence, exposure therapy, where clients gradually confronts the feared stimulus without aversive consequences, utilises fear extinction. This is supported by exposure therapy studies showing: (a) improvements in public speaking fears correlated with increased vmPFC activity (Ball et al., 2018); and (b) deficits in extinction networks and increased amygdala activity to threat normalised (Helpman et al., 2016). Consequently, pharmacological adjuncts [D-Cycloserine (DCS), cortisol, yohimbine and propranolol] and non-pharmacological adjuncts (brain stimulation, exercise) has been researched to optimise fear extinction in exposure therapy.
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
a) DCS
Firstly, DCS, a partial NDMA receptor antagonist with minimal side effects, has been found to improve exposure therapy: Ressler et al. (2004) found that combining exposure therapy for heights (virtual floor exposure) with DCS improved treatment (relative to placebo). However, subsequent studies across other anxiety disorders have been inconsistent: Cochrane meta-analysis across 22 DCS studies found that whilst some trials showed efficacy, the effects were heterogeneous, with an overall null effect (Ori et al., 2015). Nonetheless it is suggested that the heterogeneity might be because of timing of DCS and dose, and that DCS might lead to more rapid response to exposure rather than magnitude.
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
b) Cortisol
Enhanced negative feedback inhibition of cortisol in the HPA axis is found in anxiety disorders and PTSD, leading to lower chronic levels of cortisol and a “brake” on sympathetic arousal. Increasing cortisol might facilitate fear extinction learning — A recent RCT revealed greater spider fear reduction and arousal with administration of hydrocortisone prior to exposure therapy relative to placebo (Soravia et al., 2014). Similarly, administering hydrocortisone during exposure therapy has been found to reduce PTSD symptoms, increase treatment retention, and an association between reduction in PTSD symptoms and glucocorticoid receptor sensitivity was found, providing biological evidence (Yehuda et al., 2015). While cortisol appears promising, when Yehuda et al. (2015) replicated the study in a larger sample she found no significant effects.
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
c) NA
Although noradrenaline (NA) increases arousal and activation of fear-conditioning networks (e.g., amygdala), animal studies have found that NA agents (e.g., yohimbine) facilitate both fear conditioning and extinction. However, an RCT across 26 PTSD patients found no significant effects of yohimbine in facilitating exposure therapy (Tuerks et. al., 2018). Nonetheless, this was only one study.
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
d) Brain stimulation
Brain stimulation, such as tDCS and TMS, operates on the premise that since prefrontal activity is impaired in anxiety disorders, stimulation might result in enhanced function, improving fear extinction. However, Abend et al. (2015) found that tDCS instead lead to greater arousal and increased fear generalisation. Overall, the challenges for brain stimulation are: (a) difficulty to stimulate deep brain regions; and (b) patient attrition due to discomfort associated with brain stimulation. Nonetheless, it might be promising if reliable effects can be found.
Describe one mechanism that is proposed to underlie exposure therapy for anxiety disorders
and PTSD and explain how it can be applied to optimize exposure therapy.
e) Exercise
Lastly, exercise has been proposed as a way because exercise increases Brain-Derived Neurotrophic Factor (BDNF), which facilitates fear extinction learning and activate prefrontal networks. In Felmingham et al. (2013), individuals with low-expression BDNFVal66Met polymorphism displayed significantly poorer responses to exposure therapy, accounting for a high proportion of variance (14%) in treatment response. Exercise is advantageous because: (a) implementation (as compared to drugs or brain stimulation) is more acceptable to both client and patient; (b) since anxiety disorders comorbid with other psychological disorders, exercise can aid multiple disorders simultaneously.
