Memory In Posttraumatic Stress Disorder Research Articles

What Happened in the Hippocampal Axon in a Rat Model of Posttraumatic Stress Disorder.

Studies from postmortem and animal models have revealed altered synapse morphology and function in the brain of posttraumatic stress disorder (PTSD). And the effects of PTSD on dendrites and spines have been reported, however, the effection on axon include microtubule (MT) and synaptic vesicles of presynaptic elements remains unknown. Hippocampus is involved in abnormal memory in PTSD. In the present study, we used the single prolonged stress (SPS) model to mimic PTSD. Quantitative real-time polymerase chain reaction (RT-qPCR) and high-throughput sequencing (GSE153081) were utilized to analyze differentially expressed genes (DEGs) in the hippocampus of control and SPS rats. Immunofluorescence and western blotting were performed to examine change in axon-related proteins. Synaptic function was evaluated by measuring miniature excitatory postsynaptic currents (mEPSCs). RNA-sequencing analysis revealed 230 significantly DEGs between the control and SPS groups. Gene Ontology analysis revealed upregulation in axonemal assembly, MT formation, or movement, but downregulation in axon initial segment and synaptic vesicles fusion in the hippocampus of SPS rats. Increased expression in tau, β-tubulin MAP1B, KIF9, CCDC40, DNAH12 and decreased expression in p-tau, stathmin suggested SPS induced axon extension. Increased protein expression in VAMP, STX1A, Munc18-1 and decreased expression in synaptotagmin-1 suggested SPS induced more SNARE complex formation but decreased ability in synaptic vesicle fusion to presynaptic active zone membrane in the hippocampus of SPS rats. Further, low mEPSC frequency in SPS rats indicated dysfunction in presynaptic membrane. These results suggest that axon extension and synaptic vesicles fusion abnormality are involved in dysfunction of PTSD.

Cognitive functioning in posttraumatic stress disorder before and after cognitive-behavioral therapy

Although substantial evidence suggests altered executive functioning and autobiographical memory in posttraumatic stress disorder (PTSD), the clinical significance of these findings remains unclear. Here, we investigated the effects of cognitive-behavioral therapy (CBT) on different aspects of cognitive functioning (working memory, interference susceptibility, conflict adaptation, autobiographical memory) in PTSD patients in a pre-post control group design with a nested cross-sectional element. Cross-sectional analyses at baseline were conducted on 58 PTSD patients, 39 traumatized (TC), and 45 non-traumatized controls (NTC). Intervention effects were investigated before and after 25 CBT sessions in 25 PTSD and 34 untreated NTC individuals assessed in parallel. At baseline, PTSD patients showed higher conflict adaptation than the NTC group and less autobiographical memory specificity than both control groups, suggesting particularly the latter to be a correlate of PTSD. No consistent evidence for treatment-induced improvements in cognitive functioning emerged on the group level or from associations between intra-individual clinical and cognitive changes. Analyses on the role of cognitive functioning on subsequent treatment effects revealed a predictive effect of backward digit span on CBT-induced reductions of depressiveness, but no other significant effects. Our findings highlight the need for further research to identify more relevant predictors of differential treatment response.

It Took Me by Surprise: Examining the Retroactive Enhancement Effect for Memory of Naturally Unfolding Events

In two experiments, we examined how accurately participants remembered details from a naturalistic, first-person perspective film, which ended with the protagonist either encountering or not encountering an unexpected detail. Participants who watched the film with the unexpected detail at the end displayed superior accuracy for preceding event details compared to those who watched a film without such a detail. This retroactive enhancement effect generalized across both visual and auditory details, but it appeared contingent upon the unexpected detail being relevant to the event’s story. The effect occurred whether participants’ memory was tested immediately or after a two-day delay. The present findings can be seen as consistent with prior work on synaptic tagging and long-term potentiation, but the phenomenon of retroactive enhancement has not been demonstrated previously for naturally unfolding events. Implications of the findings are discussed in relation to eyewitness memory and intrusive memories in post-traumatic stress disorder.

Administration of moclobemide facilitates fear extinction and attenuates anxiety-like behaviors by regulating synaptic-associated proteins in a rat model of post-traumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a long-lasting mental disorder and accompanied by worse fear extinction. Enhanced fear memory or poor fear extinction are typical features of PTSD. Dysfunction of the serotonergic neurotransmitter system is involved in numerous mental and behavioral disorders. Monoamine oxidase A (MAOA) is important in the metabolism of serotonin and play an important role in behavious. The aim of this study was to explore the change of MAOA and effect of MAOA on fear memory in PTSD. We used single prolonged stress (SPS) to create animal model of PTSD. A startle/fear box and elevated plus maze were used to observe fear memory and anxiety level, respectively. We examined the expression of MAOA and synaptic marker protein, as well as the immunological activity of MAOA in the infralimbic cortex (IL) area, which is a critical brain region involved in emotions, especially fear regulation. We found increased anxiety-like behavior, dysfunction in fear extinction, and increased MAOA in SPS rats. After treatment with moclobemide (a selective inhibitor of MAOA), SPS rats showed significantly improved fear memory and decreased anxiety-like behavior, which indicated that moclobemide could reverse fear extinction deficit and attenuate abnormally increased levels of anxiety caused by SPS in short term. On the contrary, decreased PSD-95 and SYN1 expression in the IL region were also reversed by moclobemide. These results suggest that increased MAOA play a negative role in fear extinction and levels of anxiety in PTSD, which may be involved in change in PSD-95 and SYN1.

Investigating the role of the amygdala orexin receptor 1 in memory acquisition and extinction in a rat model of PTSD

Understanding the mechanisms underlying memory is essential for the treatment of post-traumatic stress disorder (PTSD). Orexin, as a lateral hypothalamic (LH) neuropeptide, interferes with the stages of memory, primarily through the orexin receptor1 (Orx1R). The aim of this study was to evaluate the effects of amygdala Orx1R in the acquisition and extinction processes of PTSD modeled in animals.In three experiments, rats were divided into three groups: control (Naïve), shock (receiving a foot shock), and PTSD (experiencing Single prolonged stress (SPS) method). The first experiment aimed to evaluate LH activity in PTSD modeled rats. The second and third experiments aimed to evaluate the effects of Orx1R in the acquisition and extinction of fear memory in PTSD modeled animals. SB334867 (SB) or its solvent was microinjected into the amygdala and the rats were subjected to conditioning thereafter. In the second group, we used a single injection after conditioning. In the third group, we used three consecutive injections (one after each memory test). Some behaviors and Orx1R expression were evaluated.The freezing response was significantly longer in the PTSD group than on the control. Similarly, anxiety and sensitized fear were also intensified. CFos expression levels in LH was higher in the PTSD group. Inhibition of Orx1R in the amygdala significantly decreased memory acquisition, diminished anxiety, and decreased the sensitized fear in the SB group. Applying SB to the amygdala after each fear memory test significantly decreased freezing. Expression of Orx1R was significantly higher following fear conditioning.These results indicate a likely involvement of the orexin and amygdalar Orx1R in memory acquisition and in extinction of PTSD.

The Effect of Self-Reported REM Behavior Disorder Symptomology on Intrusive Memories in Post-Traumatic Stress Disorder

ABSTRACT Background: PTSD is characterised by severe sleep disturbances, which is increasingly recognised to in many cases consist of similar symptomology to sleep disorders such as REM Behaviour Disorder (RBD). The present study aimed to investigate whether different aspects of sleep quality influence intrusive memory development and whether PTSD status moderates this relationship. Participants and Methods: 34 PTSD, 52 trauma-exposed (TE) and 42 non-trauma exposed (NTE) participants completed an emotional memory task, where they viewed 60 images (20 positive, 20 negative and 20 neutral) and, two days later, reported how many intrusive memories they had of each valence category. Participants also completed three measures of sleep quality: the Pittsburgh Sleep Quality Index, the REM Behaviour Disorder Screening Questionnaire and total hours slept before each session. Results: The PTSD group reported poorer sleep quality than both TE and NTE groups on all three measures, and significantly more negative intrusive memories than the NTE group. Mediation analyses revealed that self-reported RBD symptomology before the second session mediated the relationship between PTSD status and intrusive memories. Follow-up moderation analyses revealed that self-reported RBD symptomology before the second session was only a significant predictor of intrusion in the PTSD group, though with a small effect size. Conclusions: These findings suggest that RBD symptomology is an indicator of consolidation of intrusive memories in PTSD but not trauma-exposed or healthy participants, which supports the relevance of characterising RBD in PTSD.

The neural correlates of trauma-related autobiographical memory in posttraumatic stress disorder: A meta-analysis.

Autobiographical memory (AM) refers to memories of events that are personally relevant and are remembered from one's own past. The AM network is a distributed brain network comprised largely by prefrontal medial and posteromedial cortical brain regions, which together facilitate AM. Autobiographical memories with high arousal and negatively valenced emotional states are thought to be retrieved more readily and re-experienced more vividly. This is critical in the case of trauma-related AMs, which are related to altered phenomenological experiences as well as aberrations to the underlying neural systems in posttraumatic stress disorder (PTSD). Critically, these alterations to the AM network have not been explored recently and have never been analyzed with consideration to the different processes of AM, them being retrieval and re-experiencing. We conducted a series of effect-size signed differential mapping meta-analyses across twenty-eight studies investigating the neural correlates of trauma-related AMs in participants with PTSD as compared with controls. Studies included either trauma-related scripts or trauma-related materials (i.e., sounds, images, pictures) implemented to evoke the recollection of a trauma-related memory. The meta-analyses revealed that control and PTSD participants displayed greater common brain activation of prefrontal medial and posteromedial cortices, respectively. Whereby the prefrontal medial cortices are suggested to facilitate retrieval monitoring, the posteromedial cortices are thought to enable the visual imagery processes of AM. Taken together, reduced common activation of prefrontal cortices may be interpreted as a bias toward greater re-experiencing, where the more salient elements of the traumatic memory are relived as opposed to retrieved in a controlled manner in PTSD.

Single prolonged stress alters neural activation in the periacqueductal gray and midline thalamic nuclei during emotional learning and memory.

Clinical and preclinical studies that have examined the neurobiology of persistent fear memory in posttraumatic stress disorder (PTSD) have focused on the medial prefrontal cortex, hippocampus, and amygdala. Sensory systems, the periaqueductal gray (PAG), and midline thalamic nuclei have been implicated in fear and extinction memory, but whether neural activity in these substrates is sensitive to traumatic stress (at baseline or during emotional learning and memory) remains unexplored. To address this, we used the single prolonged stress (SPS) model of traumatic stress. SPS and control rats were either subjected to fear conditioning (CS-fear) or presented with CSs alone (CS-only) during fear conditioning. All rats were then subjected to extinction training and testing. A subset of rats were euthanized after each behavioral stage and c-Fos and c-Jun used to measure neural activation in all substrates. SPS lowered c-Jun levels in the dorsomedial and lateral PAG at baseline, but the elevated c-Jun expression in the PAG during emotional learning and memory. SPS also altered c-Fos expression during fear and extinction learning/memory in midline thalamic nuclei. These findings suggest changes in neural function in the PAG and midline thalamic nuclei could contribute to persistent fear memory induced by traumatic stress. Interestingly, SPS effects were also observed in animals that never learned fear or extinction (i.e., CS-only). This raises the possibility that traumatic stress could have broader effects on the psychological function that are dependent on the PAG and midline thalamic nuclei.

Eradicating war memories: Neuroscientific reality and ethical concerns

AbstractTraumatic memories of war can result in mental disorders such as post-traumatic stress disorder (PTSD). PTSD is characterized by intrusive trauma memories and severe stress responses with devastating personal and societal consequences. Current treatments teach patients to regulate trauma memories, but many experience a return of symptoms even after initially successful treatment. Neuroscience is discovering ways to permanently modify trauma memories and prevent the return of symptoms. Such memory modification techniques (MMTs) have great clinical potential but also important ethical, legal and social implications. In this article, the authors describe PTSD, the role of memory in PTSD, its effects on the brain, and the limitations of current treatment methods. Then, the state of the art of the neuroscience of MMTs is presented. Within this realistic scientific framework the authors will discuss the ethical, legal and social implications of MMTs for the treatment of war-induced PTSD, especially in a military population. Three major sets of issues will be focused on: safety and social justice concerns, concerns about threats to authenticity and identity, and the possible legal and moral duties to retain certain memories. Finally, the article concludes that within scientific reality, concerns are limited and do not outweigh the potential benefits of developing treatments for patients.

Mechanisms Associated with the Development of Traumatic Memories in Posttraumatic Stress Disorder

Some individuals who experience psychologically traumatic events cannot process their experiences as regular memories, and these experiences develop into traumatic memories. In individuals with posttraumatic stress disorder (PTSD), fear conditioning occurs-these individuals subsequently respond to their direct traumatic experiences and to neutral stimuli. This conditioned response eventually leads to repeated re-experiencing. In this review, we discuss biological mechanisms associated with the development of traumatic memories. These mechanisms include neural networks connecting the amygdala, hippocampus, and ventromedial prefrontal cortex, as well as the hypothalamic-pituitary-adrenal axis of the endocrine system, and epigenetic changes.

A peripheral immune response to remembering trauma contributes to the maintenance of fear memory in mice

Alterations in peripheral immune markers are observed in individuals with post-traumatic stress disorder (PTSD). PTSD is characterized in part by impaired extinction of fear memory for a traumatic experience. We hypothesized that fear memory extinction is regulated by immune signaling stimulated when fear memory is retrieved. The relationship between fear memory and the peripheral immune response was tested using auditory Pavlovian fear conditioning in mice. Memory for the association was quantified by the amount of conditioned freezing exhibited in response to the conditioned stimulus (CS), extinction and time-dependent changes in circulating inflammatory cytokines. Brief extinction training with 12 CS rapidly and acutely increased circulating levels of the cytokine interleukin-6 (IL-6), downstream IL-6 signaling, other IL-6 related pro-inflammatory cytokines. Transgenic manipulations or neutralizing antibodies that inhibit IL-6 activity did not affect conditioned freezing during the acquisition of fear conditioning or extinction but significantly reduced conditioned freezing 24 h after extinction training with 12 CS. Conversely, conditioned freezing after extinction training was unchanged by IL-6 inhibition when 40 CS were used during the extinction training session. In addition to effectively diminishing conditioned freezing, extinction training with 40 CS also diminished the subsequent IL-6 response to the CS. These data demonstrate that IL-6 released following fear memory retrieval contributes to the maintenance of that fear memory and that this effect is extinction dependent. These findings extend the current understanding for the role of the immune system in PTSD and suggest that IL-6 and other IL-6 related pro-inflammatory cytokines may contribute to the persistence of fear memory in PTSD where fear memory extinction is impaired.

Hypothesis: The Psychedelic Ayahuasca Heals Traumatic Memories via a Sigma 1 Receptor-Mediated Epigenetic-Mnemonic Process.

Ayahuasca ingestion modulates brain activity, neurotransmission, gene expression and epigenetic regulation. N,N-Dimethyltryptamine (DMT, one of the alkaloids in Ayahuasca) activates sigma 1 receptor (SIGMAR1) and others. SIGMAR1 is a multi-faceted stress-responsive receptor which promotes cell survival, neuroprotection, neuroplasticity, and neuroimmunomodulation. Simultaneously, monoamine oxidase inhibitors (MAOIs) also present in Ayahuasca prevent the degradation of DMT. One peculiarity of SIGMAR1 activation and MAOI activity is the reversal of mnemonic deficits in pre-clinical models. Since traumatic memories in post-traumatic stress disorder (PTSD) are often characterised by “repression” and PTSD patients ingesting Ayahuasca report the retrieval of such memories, it cannot be excluded that DMT-mediated SIGMAR1 activation and the concomitant MAOIs effects during Ayahuasca ingestion might mediate such “anti-amnesic” process. Here I hypothesise that Ayahuasca, via hyperactivation of trauma and emotional memory-related centres, and via its concomitant SIGMAR1- and MAOIs- induced anti-amnesic effects, facilitates the retrieval of traumatic memories, in turn making them labile (destabilised). As Ayahuasca alkaloids enhance synaptic plasticity, increase neurogenesis and boost dopaminergic neurotransmission, and those processes are involved in memory reconsolidation and fear extinction, the fear response triggered by the memory can be reprogramed and/or extinguished. Subsequently, the memory is stored with this updated significance. To date, it is unclear if new memories replace, co-exist with or bypass old ones. Although the mechanisms involved in memory are still debated, they seem to require the involvement of cellular and molecular events, such as reorganisation of homo and heteroreceptor complexes at the synapse, synaptic plasticity, and epigenetic re-modulation of gene expression. Since SIGMAR1 mobilises synaptic receptor, boosts synaptic plasticity and modulates epigenetic processes, such effects might be involved in the reported healing of traumatic memories in PTSD patients. If this theory proves to be true, Ayahuasca could come to represent the only standing pharmacological treatment which targets traumatic memories in PTSD. Lastly, since SIGMAR1 activation triggers both epigenetic and immunomodulatory programmes, the mechanism here presented could help understanding and treating other conditions in which the cellular memory is dysregulated, such as cancer, diabetes, autoimmune and neurodegenerative pathologies and substance addiction.

Neural responses to emotional involuntary memories in posttraumatic stress disorder: Differences in timing and activity.

BackgroundInvoluntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval.MethodsTwenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses.ResultsCompared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli.ConclusionsThe similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD.

Is autonoetic recollection of threat in PTSD related to impaired inhibitory skills?

IntroductionIntrusive traumatic reminiscences are among the most distressing and salient characteristics of post-traumatic stress disorder (PTSD). Associated with involuntary onsets, emotional disturbances and consciousness-related impairments, such symptoms suggest that memory functioning could be impaired in PTSD. While there is a growing body of research on experimental assessments of memory in patients with PTSD, inconsistent results remain.ObjectiveUsing an experimental methodology, this study aims to measure memory in PTSD in consideration of central features of intrusive symptoms, especially emotional, inhibitory and consciousness-related memory impairments.Method34 patients diagnosed with PTSD were compared with 37 non-PTSD controls on an item-cued directed forgetting paradigm for emotional words combined with a remember/know recognition procedure.ResultsResults confirmed prior findings of an increased and peculiarly conscious recognition of trauma-related words in PTSD. Interestingly, our results showed that, despite general memory inhibitory deficits, PTSD patients, if requested, presented a preserved ability to inhibit this improved recollection of trauma-related words.ConclusionWhile our findings highlight a biased memory functioning in favour of threatening stimuli in PTSD, inhibitory deficits for such information was not reported to play a role on this effect. Conversely, it seems that instead of inhibitory deficits, patients presented a preferential treatment of threat concordant with vigilant-avoidant models of information processing. Focusing on memory impairment in treatment for PTSD appears of prime importance. Our findings regarding preserved inhibitory skills for threat memories in the disorder could be an interesting clue for therapeutic interventions on intrusive symptoms.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Trauma-related memories in PTSD after interpersonal violence: an ambulatory assessment study

ABSTRACTBackground: Ambulatory assessment (AA) is increasingly recommended for assessing symptoms of posttraumatic stress disorder (PTSD). Previous AA studies provided new insights into the phenomenology of trauma-related memories, but also divergent findings. Notably, the range of trauma-related memories (a major target of psychotherapeutic interventions) reported in AA studies was as wide as 7.3 to 74.5 per week which might result from different methods used in these studies.Objective: We aimed at assessing the frequency of trauma-related memories in PTSD related to interpersonal violence and investigated whether this frequency is dependent upon the method.Method: For each patient trauma-related memories were assessed using two variants of smartphone-based AA: (1) Event-based sampling (EBS), i.e. participants entered data on each intrusive memory as it occurred; (2) Time-based sampling (TBS), i.e. participants reported the number of trauma-related memories they had experienced during the last two hours after they had been alerted by the smartphone. The numbers reported during the TBS-block were either analysed as reported by the participants or restricted to one per hour (rTBS). The impact of smartphone-assessments on trauma-related memories was assessed during a post-monitoring questionnaire.Results: While trauma-related memories were frequent across assessments, the methodology had a huge impact on the numbers: EBS (median = 7) and rTBS (median = 6) yielded significantly lower weekly numbers of intrusive trauma-related memories than TBS (median = 49). Accordingly, the possibility to report unrestricted numbers of trauma-related memories clearly impacted the results. The post-monitoring questionnaire identified another source for the divergent findings: while feeling disrupted by the smartphone-assessments was unrelated to the numbers reported during EBS, feeling disrupted was related to an increase of trauma-related memories during TBS and rTBS.Conclusions: The method clearly impacts the recorded number of trauma-related memories. Future research should clarify whether other variables (e.g. the subjective stress related to intrusive memories) are less dependent on the methodology.

La mémoire intrusive dans le trouble de stress post-traumatique : apport de la neuroimagerie

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that develops in individuals who have been exposed to life-threatening events. The current definitions are more extensive, including people indirectly involved. This last point means that the role of memory and mental imagery is major and also explains that flashback and intrusive memory are core symptoms of the disorder. If most people experience intrusive memories after witnessing or experiencing a traumatic event, not everyone develops PTSD. We need more knowledge about how involuntary images of the trauma intrude into consciousness as intrusive memories. Memory process is well documented, however little is known about specific context of traumatic memory. Brain imaging has been used extensively in the exploration of this disorder, but more data is needed to establish differential psychology between subjects, to make prediction of transition to PTSD, or that can orient the specific therapeutic choice. Investigating subjects during a traumatic event is methodologically complex and ethically unfeasible. It can be experimentally induced using an experimental analogue to approach real-life conditions. We propose in this article a focus on the intrusive memories in PTSD and describe the main outcomes from clinical neurosciences studies.

The role of memory in posttraumatic stress disorder: implications for clinical practice.

Posttraumatic stress disorder (PTSD) is a highly prevalent disorder with important social consequences. Several models have been developed with the aim of understanding the mechanisms underlying its symptoms. Intrusions are idiosyncratic symptoms that commonly take the form of involuntary recollection of images or flashbacks about the traumatic event. To review how memory is conceptualized in each of these models and the implications for clinical practice. A narrative review of the literature was conducted through analysis of the perspectives of memory in theoretical models of PTSD. Two main perspectives were identified: 1) models in which specific mechanisms of memory for processing traumatic events are proposed, especially those based on clinical studies, and 2) models in which common mnemonic mechanisms are utilized to explain the phenomenon, primarily based on basic experimental research studies investigating memory. The different theories based on these approaches have led to distinct psychotherapy interventions. In order to clarify these discrepancies, future research should aim for the methodological rigor of experimental studies, while maintaining the ecological applicability of findings. Cognitive experimental psychopathology is therefore an area on which research funding should be focused. Such studies could elucidate the role of mnemonic aspects in PTSD and how they impact psychological treatments.

PTSD symptoms lead to modification in the memory of the trauma: a prospective study of former prisoners of war.

With the growing interest in the role of trauma memory in posttraumatic stress disorder (PTSD), this prospective study examined long-term changes in memory and the bidirectional relationship between symptoms of PTSD and trauma memory. A sample of Israeli former prisoners of the 1973 Yom Kippur War (N = 103) was assessed in 1991 and in 2008. Participants' PTSD symptom clusters, measured by the PTSD Inventory, and recollections of subjective and objective exposure during captivity, measured by a self-report questionnaire, were assessed at both times. Data on prewar and postwar negative life events and psychotherapy were also collected. Repeated-measures analysis revealed that participants' recollections were increasingly negative over time (P < .001). Applying an autoregressive cross-lagged modeling strategy showed that the PTSD symptoms of hyperarousal facilitated subsequent amplifications in their recollections (P < .01). These findings challenge the accuracy of reports of traumatic experiences and show that PTSD symptoms, in part, lead to the formation of more negative recollections over time. The findings suggest that the original memory is repeatedly updated under the influence of the individual's emotional state. The findings are discussed in the context of the reconsolidation theory of memory.

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

BackgroundPropranolol 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. MethodWithin a randomized double-blind placebo controlled trial, propranolol's 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). ResultsThe 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. LimitationsThe 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 propranolol's effect on PTSD associated cognitive impairment. ConclusionsOur 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.

Visual false memories in posttraumatic stress disorder.

This study investigated visual false memories in posttraumatic stress disorder (PTSD). The Scenic False Memory paradigm (SFM, Hauschildt, Peters, Jelinek, & Moritz, 2012) was administered to male Iranian military personnel who had participated in the Iran-Iraq war and were diagnosed with (n = 21) or without (n = 21) PTSD and a sample of healthy male non-trauma-exposed controls (n = 21). Trauma-exposed participants recalled and recognized a significantly lower percentage of hits and a significantly greater percentage of false memories for both trauma-related and non-trauma-related video scenes, than non-trauma-exposed controls. Among the trauma-exposed participants, those with and without PTSD did not differ significantly in terms of percentage of hits and false memories recalled on the SFM. Those with PTSD were found to recognize significantly fewer hits for both the trauma-related and non-trauma-related videos than those without PTSD. Those with PTSD also recognized significantly more false memories for the trauma video scene than the non-PTSD group. The findings suggest that those with trauma exposure, and in particular those with PTSD, may have a greater susceptibility to visual false memory.