Trauma reactivation under the influence of propranolol: An examination of clinical predictors

Université de Montréal, Montréal, QC, Canada.
European Journal of Psychotraumatology (Impact Factor: 2.4). 02/2012; 3. DOI: 10.3402/ejpt.v3i0.15470
Source: PubMed


In two recent studies conducted by our group, a treatment combining propranolol with a brief reactivation session subsequently reduced posttraumatic stress disorder (PTSD) symptom severity and diagnosis, as well as reducing psychophysiological responses during trauma-related script-driven imagery. One likely explanation for those results is that memory reconsolidation was blocked by propranolol.
We explored the influence of various predictors on treatment outcome (i.e., PTSD severity), and whether the treated individuals improved in other important domains of functioning associated with PTSD.
Thirty-three patients with longstanding PTSD participated in a 6-week open-label trial consisting of actively recalling one's trauma under the influence of propranolol, once a week.
Treated patients reported a better quality of life, less comorbid depressive symptoms, less negative emotions in their daily life and during trauma recollections. Women were also found to improve more than men. Type of trauma (childhood vs. adulthood), time elapsed since trauma, borderline personality traits, depressive symptoms severity, Axis I comorbidity, and age did not influence treatment outcome.
These results must await publication of a randomized-controlled trial to further delineate effectiveness with this novel treatment approach.

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Available from: Alain Brunet, Feb 19, 2015
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    • "However, memory reconsolidation blockade has shown promise in animal models of drug dependence (e.g., Przybyslawski et al. 1999), indicating that more work may be needed to translate the animal model of drug dependence to a therapeutic intervention that can be tested the clinic. It may be premature to rule out an inhibitory role for propranolol in reconsolidation blockade of smoking-related memories until trials are done in recently abstinent smokers, with a range of doses (e.g., Poundja et al. 2012) and with repeated propranolol administration in order to detect whether a greater, longer lasting effect of reconsolidation blockade on smoking-related memories can be obtained. "
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    ABSTRACT: Smoking cue exposure reactivates salient smoking-related memories, triggering craving to smoke, a phenomenon associated with maintenance of smoking behavior and relapse after periods of abstinence. Acute β-adrenergic blockade with propranolol reduces physiologic reactivity during subsequent recollection of traumatic events by inhibiting reconsolidation of reactivated memories in a process called memory reconsolidation blockade. The objective of this study is to determine whether a single dose of propranolol prior to retrieval of smoking-related memories reduces subsequent physiologic reactivity to personally salient smoking imagery scripts in current smokers. Fifty-four overnight-abstinent, adult smokers received a single-dose propranolol or placebo prior to reactivation of smoking-related memories in a randomized, double-blind, placebo-controlled trial and resumed smoking afterward. One week later, skin conductance (SC), heart rate (HR), left corrugator electromyogram (EMG), self-reported emotional state, and craving were assessed following script-driven imagery with neutral and personalized smoking-related scripts. Smoking scripts were associated with increased physiologic activation (SC, HR, EMG), craving, and negative emotional state compared with neutral scripts. Propranolol did not moderate the effect of script type on any outcome. Personalized smoking script-driven imagery robustly increased physiologic activation, negative emotional state, and craving, and a single dose of propranolol prior to memory reactivation did not moderate this effect.
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    • "Second, reconsolidation disruption by noradrenergic receptor antagonism is memory specific and does not eliminate associated or nonreactivated memories (Bernardi et al, 2006; Kindt et al, 2009; Otis et al, 2013; Przybyslawski et al, 1999; Soeter and Kindt, 2011). Third, noradrenergic receptor blockade during reconsolidation has been shown to improve quality of life in patients with PTSD (Brunet et al, 2011; Poundja et al, 2012). Finally, noradrenergic receptor blockade during reconsolidation is capable of reducing cue-induced drug cravings (Saladin et al, 2013), suggesting that such therapy could limit relapse susceptibility. "
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    ABSTRACT: Emotional and traumatic experiences lead to the development of particularly strong memories that can drive neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD) and drug addiction. Disruption of these memories would therefore serve as a powerful treatment option, and targeting the pathologic emotional, but not declarative, component of a memory would be ideal for clinical intervention. Research reveals that after retrieval of a consolidated memory, the memory can be destabilized, and must then be reconsolidated through synaptic plasticity to allow subsequent retrieval. Disruption of reconsolidation-related plasticity would therefore impair specific, reactivated memories. Noradrenergic signaling strengthens synaptic plasticity and is essential for encoding the emotional components of memory. Consistent with this, investigations have now revealed that noradrenergic signaling is a critical mechanism for reconsolidation of emotional memories in rodent and human models. Here, we discuss these investigations and promising clinical trials indicating that disruption of noradrenergic signaling during reconsolidation may abolish the pathologic emotional, but not declarative, component of memories allowing alleviation of neuropsychiatric disorders including PTSD and drug addiction.
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    • "Furthermore, McDonagh et al. (2005) found that a comorbid BPD/PTSD was related to dropout of CBT, suggesting that difficulties with interpersonal and emotional regulation could contribute to negative outcome. It should be noted that these findings have not consistently been replicated (Clarke, Rizvi, & Resick, 2008; Poundja, Sanche, Tremblay, & Brunet, 2012). However, BPD patients tend to be excluded from PTSD treatment trials (Bradley et al., 2005), especially those with more severe symptomatology (e.g., acute self-harming behavior). "
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    ABSTRACT: Posttraumatic stress disorder (PTSD) represents an often chronic and debilitating mental illness resulting from exposure to trauma. Although the most compelling evidence for the treatment of PTSD is cognitive behavioral therapy (CBT), many patients experience residual functional impairment, or relapse, suggesting that this approach does not work for all cases of PTSD. Repeated severe trauma, particularly during development, might increase the risk for a more intricate clinical profile, called complex PTSD (CPTSD), which might contribute to poorer treatment response. The following provides a comprehensive summary of the evidence examining whether CPTSD symptomatology is related to poorer treatment outcome of CBT, reviews the literature on the treatment of CPTSD, and offers insights into current issues and future directions of the construct.
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