Psychosocial therapy for posttraumatic stress disorder [Supplement 2]

Center for the Treatment and Study of Anxiety, University of Pennsylvania, Philadelphia, PA 19104, USA.
The Journal of Clinical Psychiatry (Impact Factor: 5.5). 02/2006; 67 Suppl 2:40-5.
Source: PubMed


Immediately after experiencing a traumatic event, many people have symptoms of posttraumatic stress disorder (PTSD). If trauma victims restrict their routine and systematically avoid reminders of the incident, symptoms of PTSD are more likely to become chronic. Several clinical studies have shown that programs of cognitive-behavioral therapy (CBT) can be effective in the management of patients with PTSD. Prolonged exposure (PE) therapy-a specific form of exposure therapy-can provide benefits, as can stress inoculation training (SIT) and cognitive therapy (CT). PE is not enhanced by the addition of SIT or CT. PE therapy is a safe treatment that is accepted by patients, and benefits remain apparent after treatment programs have finished. Nonspecialists can be taught to practice effective CBT. For the treatment of large numbers of patients, or for use in centers where CBT has not been routinely employed previously, appropriate training of mental health professionals should be performed. Methods used for the dissemination of CBT to nonspecialists need to be modified to meet the requirements of countries affected by the Asian tsunami. This will entail the use of culturally sensitive materials and the adaptation of training methods to enable large numbers of mental health professionals to be trained together.

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    • "Importantly, there are several studies suggesting that fear extinction is impaired in individuals with anxiety disorders [28] [29] [30] [31]. Therefore, to promote extinction learning, the patient in exposure therapy is repeatedly given actual (in vivo exposure) or imaginary exposure to the trauma-associated cues or contexts followed by relaxation in order to reduce the negative emotional response elicited by these stimuli [32] [33] [34]. Exposure therapies have been successfully used to treat anxiety disorders since the work of Wolpe and co-workers in 1960s ([35] [36]; see [37] for a historical perspective) and they continue to be the most effective treatment method for a variety of anxiety disorders. "
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    ABSTRACT: Anxiety disorders are a group of crippling mental diseases affecting millions of Americans with a 30% lifetime prevalence and costs associated with healthcare of $42.3 billion. While anxiety disorders show high levels of co-morbidity with smoking (45.3% vs. 22.5% in healthy individuals), anxiety disorders are also more common among the smoking population (22% vs. 11.1% in the non-smoking population). Moreover, there is clear evidence that smoking modulates symptom severity in patients with anxiety disorders. In order to better understand this relationship, several animal paradigms are used to model several key symptoms of anxiety disorders; these include fear conditioning and measures of anxiety. Studies clearly demonstrate that nicotine mediates acquisition and extinction of fear as well as anxiety through the modulation of specific subtypes of nicotinic acetylcholine receptors (nAChRs) in brain regions involved in emotion processing such as the hippocampus. However, the direction of nicotine's effects on these behaviors is determined by several factors that include the length of administration, hippocampus-dependency of the fear learning task, and source of anxiety (novelty-driven vs. social anxiety). Overall, the studies reviewed here suggest that nicotine alters behaviors related to fear and anxiety and that nicotine contributes to the development, maintenance, and reoccurrence of anxiety disorders. Copyright © 2015. Published by Elsevier Inc.
    Biochemical pharmacology 07/2015; 97(4). DOI:10.1016/j.bcp.2015.07.029 · 5.01 Impact Factor
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    • "This appears to be caused by a failure of consolidating and recalling extinction memory that most likely originates from a mPFC dysfunction (Rauch et al., 2006; Etkin, 2012). Since exposure therapy as an effective treatment for anxiety disorders (Foa, 2006) represents the implementation of extinction , it is of clinical relevance to improve extinction learning and extinction memory consolidation. In this regard, manipulations of memory consolidation processes have been established in cross-species translational research. "
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    ABSTRACT: The extinction of conditioned fear depends on an efficient interplay between the amygdala and the medial prefrontal cortex (mPFC). In rats, high-frequency electrical mPFC stimulation has been shown to improve extinction by means of a reduction of amygdala activity. However, so far it is unclear whether stimulation of homologues regions in humans might have similar beneficial effects. Healthy volunteers received one session of either active or sham repetitive transcranial magnetic stimulation (rTMS) covering the mPFC while undergoing a 2-day fear conditioning and extinction paradigm. Repetitive TMS was applied offline after fear acquisition in which one of two faces (CS+ but not CS-) was associated with an aversive scream (UCS). Immediate extinction learning (day 1) and extinction recall (day 2) were conducted without UCS delivery. Conditioned responses (CR) were assessed in a multimodal approach using fear-potentiated startle (FPS), skin conductance responses (SCR), functional near-infrared spectroscopy (fNIRS), and self-report scales. Consistent with the hypothesis of a modulated processing of conditioned fear after high-frequency rTMS, the active group showed a reduced CS+/CS- discrimination during extinction learning as evident in FPS as well as in SCR and arousal ratings. FPS responses to CS+ further showed a linear decrement throughout both extinction sessions. This study describes the first experimental approach of influencing conditioned fear by using rTMS and can thus be a basis for future studies investigating a complementation of mPFC stimulation to cognitive behavioral therapy (CBT).
    Frontiers in Behavioral Neuroscience 02/2014; 8:44. DOI:10.3389/fnbeh.2014.00044 · 3.27 Impact Factor
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    • "Exposure therapy is the most common behavioral treatment for patients with post-traumatic stress disorder (PTSD) (Foa, 2006). Procedurally, it is similar to the fear extinction paradigm in rodents, involving exposure to a series of conditional stimulus (CS). "
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    ABSTRACT: Extinction is a well-known and important behavioral phenomenon that allows an organism to adapt its behavior to its environment. Previous studies have shown that the expression of extinction is highly context dependent, meanwhile, conditioning context, as part of fear memory, might have influence on extinction formation. To this end, we have conducted four different extinction paradigms in this study: extinction conducted in the conditioning context but tested in another, novel context (AAB); conditioning in one context and extinction and testing in the second (ABB); conditioning in context A, extinction training in context B, but test back to context A (ABA); and extinction training in a third context, context C (ACB). Additionally, a low dose of the GABAA agonist muscimol was used to temporarily inactivate CA1 to observe its effect in extinction. Our results showed that rats under the AAB, but not the ACB or ABA condition, showed a similar level of freezing compared with the typical ABB extinction paradigm. Moreover, muscimol infused into CA1 before extinction training resulted in impaired extinction and down-regulation of NR2B activity and phosphorylated GluR1 (at Ser845) in CA1, and the expression levels of NR2B and GluR1 were decreased significantly in the BLA. Thus, CA1 may play an important role in the context-specific expression of fear extinction, and Ser845 may be a phosphorylation site in GluR1 in CA1, triggering the context-specific response of extinction memory.
    Neuroscience 12/2013; 260. DOI:10.1016/j.neuroscience.2013.12.014 · 3.36 Impact Factor
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