Andrea R. Ashbaugh

Trauma reactivation plus propranolol is associated with durably low physiological responding during subsequent script-driven traumatic imagery.

Objective: In a previous, double-blind, placebo-controlled study, patients with posttraumatic stress disorder (PTSD) showed lower physiological response during script-driven traumatic imagery 1 week after receiving a single dose of propranolol given after the retrieval of a traumatic memory. We hypothesized that this effect would extend beyond 1 week using a modified treatment approach. Method: Twenty-eight participants with PTSD read an account of their traumatic event once weekly for 6 consecutive weeks under the influence of open-label propranolol. One week and 4-months later, skin conductance, heart rate, and left corrugator electromyogram responses were measured while participants engaged in script-driven mental imagery of their traumatic event. Results from the 22 study participants were compared with results from treated and untreated participants in a previously published trial. Results: Most participants in our study were classified as non-PTSD cases at posttreatment and follow-up according to a psychophysiological discriminant function analysis. Posttreatment skin conductance and heart rate responses of the current (propranolol-treated) participants were lower than those of placebo participants from the previous study. No difference was observed between physiological responding measured posttreatment and at follow-up. Conclusions: Low physiological responding during script-driven traumatic imagery after treatment extends up to 4 months, demonstrating the durability of the treatment effects. Limitations include the absence of a placebo-controlled group and lack of physiological baseline measures. Despite these limitations, results point to the need for future trials examining the clinical efficacy of trauma reactivation plus propranolol, as it has the potential to become a novel, cost- and time-effective treatment for PTSD.

Does reconsolidation occur in humans: a reply

Schiller and Phelps (2011) have provided a thoughtful and comprehensive review in the May issue of Frontiers in Behavioral Neurosciences entitled, “Does reconsolidation occur in humans?” This scholarly paper captures many of the challenges in translating the animal research on reconsolidation to humans. We agree with their main argument that there is little published evidence in humans that meets one important reconsolidation criterion, namely, that the memory-weakening treatment should be administered after the memory reactivation, so as not to influence the preceding memory retrieval process. However, it is unclear whether pre-reactivation propranolol significantly hampers memory retrieval. On the basis of this uncertainty, Schiller and Phelps go on to suggest that the memory impairing effects of pre-reactivation propranolol (e.g., Kindt et al., 2009; Brunet et al., 2011) must be explained by some process other than reconsolidation. Such a conclusion appears illogical, because if propranolol does not impair retrieval sufficiently to preclude reconsolidation, then blockade of memory reconsolidation remains a viable explanation for pre-reactivation propranolols memory-weakening action. Indeed, the ultimate evidence for successful memory retrieval is measured during reactivation (e.g., freezing behavior in rodent fear conditioning, GSR in human fear conditioning, etc.). Therefore, any impairment of retrieval should be detected. Moreover, as shown recently by Debiec et al. (2011) immediate post-retrieval beta-adrenergic receptor stimulation enhances reconsolidation of fear conditioning in the amygdala. In this scenario, administration of propranolol following memory retrieval (which results in arousal and noradrenergic stimulation) may be too late to be effective. So, a parsimonious explanation is that pre-reactivation propranolol did block reconsolidation to some extent in the above-mentioned studies. Pre-reactivation propranolol studies (and other studies with a similar design) ought to be pursued vigorously because, irrespective of how the memory impairing effect is obtained, they offer the prospect of a novel approach to treating mental disorders that have at their core an emotional, usually traumatic, memory. Although Schiller and Phelps acknowledge some of the challenges of blocking reconsolidation using pharmacological means in humans, it is important to note the reasons for this difficulty. In animals, reconsolidation (i.e., protein synthesis) is believed to begin 3–10 min after memory reactivation (Monfils et al., 2009). Most of it appears to take place within the first 2 h (Przybyslawski et al., 1999) and to be over by the sixth hour (Duvarci and Nader, 2004). Considering that oral propranolol takes about 90 min to reach its peak bioavailability in human blood (Marino, 1987); and considering that only a fraction of this drug will eventually cross the blood–brain barrier to be available to exert the necessary effect, protocols that use post-reactivation propranolol are vulnerable to yielding negative results because not enough protein synthesis will have been blocked by the time the drug reaches its full effect in the human brain. Since conducting our proof-of-concept study in posttraumatic stress disorder (PTSD; Brunet et al., 2008), which used post-reactivation propranolol, we have opted to use pre-reactivation propranolol in an attempt to develop what we hope will be a more potent therapeutic protocol (see Brunet et al., 2011). It is unfortunate that this type of protocol does not meet an important scientific criterion for studies that use it to be labeled as genuine “reconsolidation” studies, but this is the price to pay for conducting sound translational research in patients. Schiller et al. (2010) are to be commended for their efforts to devise a human protocol that circumvents the problems associated with pharmacological blockade of reconsolidation by incorporating new material into a destabilized old memory, rather than simply blocking its reconsolidation. However, they have yet to show that such an approach is sufficiently potent to help patients overcome their psychological symptoms stemming from a traumatic emotional memory.

Psychometric Validation of the English and French Versions of the Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5).

The purpose of this study is to assess the psychometric properties of a French version of the Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5), a self-report measure of posttraumatic stress disorder (PTSD) symptoms, and to further validate the existing English version of the measure. Undergraduate students (n = 838 English, n = 262 French) completed the PCL-5 as well as other self-report symptom measures of PTSD and depression online. Both the English and French versions PCL-5 total scores demonstrated excellent internal consistency (English: α = .95; French: α = .94), and strong convergent and divergent validity. Strong internal consistency was also observed for each of the four subscales for each version (α’s > .79). Test-retest reliability for the French version of the measure was also very good (r = .89). Confirmatory factor analysis indicated that the four-factor DSM-5 model was not a good fit of the data. The seven-factor hybrid model best fit the data in each sample, but was only marginally superior to the six-factor anhedonia model. The French version of the PCL-5 demonstrated the same psychometric qualities as both the English version of the same measure and previous versions of the PCL. Thus clinicians serving French-speaking clients now have access to this highly used screening instrument. With regards to the structural validity of the PCL-5 and of the new PTSD diagnostic structure of the DSM-5, additional research is warranted. Replication of our results in clinical samples is much needed.

The decision to vaccinate or not during the H1N1 pandemic: selecting the lesser of two evils?

Background With the release of the H1N1 vaccine, there was much controversy surrounding its use despite strong encouragements to be vaccinated in the media. Though studies have examined factors influencing peoples decision to be vaccinated, few have focused on how general beliefs about the world or where an individual gathers information might influence that decision. Methodology/Principal Findings A cross-sectional web-based survey (N = 817) was conducted during the H1N1 outbreak after the vaccine was available. Variables examined included sociodemographic information, health related behaviours, specific beliefs concerning the H1N1 virus and its vaccine, as well as general beliefs, such as fear of contamination, intolerance of uncertainty, emotional states, coping behaviour, and the source of information concerning the virus. Three converging statistical methods were used to examine the associations – analysis of variance, logistic regression, and recursive partition modelling. The most consistent and strongest association was that negative beliefs about the H1N1 vaccine (e.g. fear of its side effects) was related to the decision not to be vaccinated, whereas beliefs about the dangers of the H1N1 virus was related to the decision to be vaccinated. Most notably, having very strong negative beliefs about the vaccine was a more powerful predictor than even strong beliefs about the dangers of the H1N1 virus. Furthermore, obtaining information from the Internet, as compared to more traditional sources of information (e.g., TV, newspapers) was related to the decision not to be vaccinated. Conclusions/Significance These results are consistent with the Health Belief Model. Importantly they suggest that during future pandemics public health officials should not only discuss the dangers of the pandemic but also (i) take additional steps to reassure the public about the safety of vaccines and (ii) monitor the information disseminated over the Internet rather than strictly relying on the more traditional mass media.

The impact of depression and PTSD symptom severity on trauma memory

ABSTRACT Posttraumatic stress disorder (PTSD) and depression frequently co-occur following a traumatic event. Differences in the processing of autobiographical memory have been observed in both disorders in the form of overgeneralised memories and negative intrusive memories. The current study examined how symptoms of PTSD and depression influence the phenomenological characteristics of trauma memories. Undergraduate students who had experienced a traumatic event (n = 696) completed questionnaires online including measures of PTSD and depressive symptom severity. They rated their trauma memory on several phenomenological characteristics using the Memory Experiences Questionnaire [Sutin, A. R., & Robins, R. W. (2007). Phenomenology of autobiographical memories: The memory experiences questionnaire. Memory.]. Moderated multiple regression was used to examine how PTSD and depressive symptom severity related to each phenomenological characteristic. Symptoms of PTSD and depression were related separately and uniquely to the phenomenological characteristics of the trauma memory. PTSD severity predicted trauma memories that were more negative, contained higher sensory detail, and were more vivid. In contrast, depressive symptom severity predicted trauma memories that were less accessible and less coherent. These findings suggest that depressive and PTSD symptomatology affect traumatic memory differently and support a distinction between these two disorders.

Apathy, not depressive symptoms, as a predictor of semantic and phonemic fluency task performance in stroke and transient ischemic attack

ABSTRACT Objectives: This study examined the relationship between apathy and cognition in patients with cerebrovascular disease. Apathy may result from damage to frontal subcortical circuits causing dysexecutive syndromes, but apathy is also related to depression. We assessed the ability of apathy to predict phonemic fluency and semantic fluency performance after controlling for depressive symptoms in 282 individuals with stroke and/or transient ischemic attack. Method: Participants (N = 282) completed the Phonemic Fluency Test, Semantic Fluency Test, Center for Epidemiologic Studies Depression Scale, and Apathy Evaluation Scale. A cross-sectional correlational design was utilized. Results: Using hierarchical linear regressions, apathy scores significantly predicted semantic fluency performance (β = –.159, p = .020), but not phonemic fluency performance (β = –.112, p = .129) after scaling scores by age and years of education and controlling for depressive symptoms. Depressive symptoms entered into the first step of both hierarchical linear regressions did not predict semantic fluency (β = –.035, p = .554) or phonemic fluency (β = –.081, p = .173). Apathy and depressive symptoms were moderately correlated, r(280) = .58, p < .001. Conclusions: The results of this study are consistent with research supporting a differentiation between phonemic and semantic fluency tasks, whereby phonemic fluency tasks primarily involve frontal regions, and semantic fluency tasks involve recruitment of more extended networks. The results also highlight a distinction between apathy and depressive symptoms and suggest that apathy may be a more reliable predictor of cognitive deficits than measures of mood in individuals with cerebrovascular disease. Apathy may also be more related to cognition due to overlapping motivational and cognitive frontal subcortical circuitry. Future research should explore whether treatments for apathy could be a novel target for improving cognitive outcomes after stroke.

Propranolol's impact on cognitive performance in post-traumatic stress disorder

BACKGROUND Propranolol has effectively diminished fear-based emotional memories in posttraumatic stress disorder (PTSD) and this effect has been attributed to traumatic memory reconsolidation blockade. However, propranolol may also exert cognitive effects by modulating stress and arousal. METHOD Within a randomized double-blind placebo controlled trial, propranolols impact on cognitive functioning was examined in individuals who were diagnosed with chronic PTSD. Participants received a single dose of 1mg/kg of propranolol (n=20) or placebo (n=21), and completed subtests of the Wechsler Adult Intelligence Scale third edition (WAIS-III). PTSD symptoms were assessed 1 week before and after treatment by the Impact of Event Scale Revised (IES-R). RESULTS The propranolol group performed significantly better on the Processing Speed composite measure compared to the placebo group. Furthermore, greater heart rate decreases were associated with higher Perceptual Organization performance, within the propranolol group. LIMITATIONS The generalizability of results may have been reduced as participants were treatment seeking; the sample size was small and included a greater proportion of females.This study could not assess whether pre-existing psychological function influenced cognitive performance, post-trauma. Future studies might consider including a non-PTSD control group to determine if our findings are specific to propranolols effect on PTSD associated cognitive impairment. CONCLUSIONS Our preliminary results demonstrated that cognitive functioning improved following propranolol administration in PTSD patients. The implications are discussed with regards to the processing of traumatic events.

Hoping for more: How cognitive science has and hasn't been helpful to the OCD clinician

Cognitive-behavioural models of obsessive-compulsive disorder (OCD) stemmed from knowledge acquired from cognitive science. Researchers continue to apply basic cognitive-affective science methods to understanding OCD, with the overarching goal of improving and refining evidence-based treatments. However, the degree to which such research has contributed to this goal is unclear. We reviewed OCD research in the general areas that comprise basic cognitive science, and evaluated the degree to which it has contributed to our understanding of the development, maintenance, and treatment of OCD. We focused on studies that either compared people with and without OCD and/or used experimental psychopathology methods with human participants, and attempted to resolve some of the conflicting theories related to the importance of cognitive deficits vs. cognitive biases. Overall, we observed equivocal findings for deficits in perception, attention, memory, and executive functioning. Moreover, many so-called deficits were moderated and/or explained by OCD-relevant beliefs, highlighting the role of confidence in cognitive processes as integral to our understanding of OCD. We discussed these findings in terms of cognitive measurement, cognitive-behavioural models, and clinical applicability, and made recommendations for future research that may offer innovation and insight helpful to clinicians working to improve the symptoms and lives of people with OCD.

The Role of Apathy and Depression on Verbal Learning and Memory Performance After Stroke

OBJECTIVE Psychiatric symptoms, including depression and apathy, may significantly impede functional and cognitive capabilities following a cerebrovascular event. This study examined the role of apathy and depression on learning and memory performance in stroke patients. METHOD Stroke patients (n = 140 [119 ischemic, 21 hemorrhagic], mean age = 60.6 [SD = 15.1]) completed the Apathy Evaluation Scale (AES), the Center for Epidemiologic Studies Depression Scale (CES-D), and the California Verbal Learning Test-Second Edition (CVLT-II). RESULTS Using a 2 × 2 MANOVA with depression (CESD ≥ 16) and apathy (AES ≥ 34) as the independent variables and cognitive performance (i.e., verbal acquisition, short-term free recall, and long-term free recall) as the dependent variables, we found a main effect for apathy (F[3,134] = 2.98, p = .034), such that apathetic stroke patients (n = 24) performed significantly worse on verbal acquisition (F[1,136] = 6.44; p = .012), short-term free recall (F[1,136] = 7.86; p = .006), and long-term free recall (F[1,136] = 8.37; p = .004) than nonapathetic stroke patients (n = 116). There was no main effect of depression on cognitive performance (F[1,136] = 1.72, p = .155). CONCLUSIONS These results suggest that apathy, not depression, is related to verbal memory performance in stroke patients. Future research should explore whether treatment of apathy (e.g., improving motivation) could be a novel target for improving cognition after stroke. Researchers should also examine whether this model can be applied to other aspects of cognition, including executive function and other areas of memory including autobiographical and working memory.

Robin Shapiro, The Trauma Treatment Handbook: Protocols Across the Spectrum

Fernando, S. (1988). Race and culture in psychiatry. London, UK: Croom Helm. Fernando, S. (2005). Multicultural mental health services: Projects for minority ethnic communities in England. Transcultural Psychiatry, 42(3), 420–436. Fernando, S. (2010). Mental health, race and culture (3rd ed.). Basingstoke, UK: Palgrave Macmillan. Fernando, S. & Keating, F. (Eds.). (2009). Mental health in a multi-ethnic society: A multidisciplinary handbook (2nd ed.). London, UK: Routledge. Gaines, A. D. (1992). Ethnopsychiatry: The cultural construction of professional and folk psychiatries. New York: State University of New York Press. Kirmayer, L. (2006). Culture and psychotherapy in a creolizing world. Transcultural Psychiatry, 43(2), 163–168. Kleinman, A. (1977). Depression, somatization and the ‘‘new cross-cultural psychiatry’’. Social Science and Medicine, 11, 3–10. Leff, J. (1981). Psychiatry around the globe: A transcultural view. New York, NY: Marcel Dekker. Leighton, A. H., & Hughes, J. M. (1961). Cultures as causative of mental disorder. Millbank Memorial Fund Quarterly, 39(3), 446–470. Littlewood, R., & Lipsedge, M. (1982). Aliens and alienists: Ethnic minorities and psychiatry. Harmondsworth, UK: Penguin. Marsella, A. J. & White, G. M. (Eds.). (1982). Cultural conceptions of mental health and therapy. Dordrecht, NL: Reidel. Metzl, J. (2009). The protest psychosis: How schizophrenia became a black disease. Boston, MA: Beacon Press. Murphy, H. B. M. (1986). The historical development of transcultural psychiatry. In J. Cox (Ed.), Transcultural Psychiatry (pp. 7–22). London, UK: Croom Helm. Omi, M., & Winant, H. (1994). Racial formation in the United States, from the 1960s to the 1990s. New York, NY: Routledge. Rack, P. (1982). Race, culture and mental disorder. London, UK: Tavistock.