Non-fear emotions in changes in posttraumatic stress disorder symptoms during treatment.

BACKGROUND AND OBJECTIVES: Posttraumatic stress disorder (PTSD) is not only associated with fear but also with other emotions. The present study aimed to examine if changes in shame, guilt, anger, and disgust predicted changes in PTSD symptoms during treatment, while also testing if PTSD symptoms, in turn, predicted changes in these emotions. METHODS: Participants (N = 155) with childhood-related PTSD received a maximum of 12 sessions of eye movement desensitization and reprocessing or imagery rescripting. The data was analyzed using Granger causality models across 12 treatment sessions and 6 assessment sessions (up until one year after the start of treatment). Differences between the two treatments were explored. RESULTS: Across treatment sessions, shame, and disgust showed a reciprocal relationship with PTSD symptoms, while changes in guilt preceded PTSD symptoms. Across assessments, anger was reciprocally related to PTSD, suggesting that anger might play a more important role in the longer term. LIMITATIONS: The individual emotion items were not yet validated, and the CAPS was not administered at all assessments. CONCLUSIONS: These findings partly differ from earlier studies that suggested a unidirectional relationship in which changes in emotions preceded changes in PTSD symptoms during treatment. This is in line with the idea that non-fear emotions do play an important role in the treatment of PTSD and constitute an important focus of treatment and further research.

Dyadic Investigation of Posttraumatic Stress Symptoms and Daily Sleep Health in Patients With Cancer and Their Caregivers.

OBJECTIVE: Cancer can be a traumatic experience affecting multidimensional aspects of sleep among patients and caregivers. This study examined the differential associations of cancer-related posttraumatic stress symptoms (PTSS) with various sleep markers in this population. METHODS: Patients newly diagnosed with colorectal cancer ( n = 138, mean age = 56.93 years, 31.88% female, 60.14% Hispanic, 6.53 months after diagnosis) and their sleep-partner caregivers ( n = 138, mean age = 55.32 years, 68.12% female, 57.97% Hispanic) completed questionnaires assessing the four PTSS clusters (intrusion, avoidance, alterations in arousal and reactivity, negative alterations in cognitions and mood). Participants also completed daily sleep diaries for 14 consecutive days, from which sleep onset latency (SOL), wake after sleep onset (WASO), and sleep duration were derived. RESULTS: Actor-partner interdependence model revealed that caregivers' greater alterations in arousal and reactivity were associated with their own longer SOL ( b = 15.59, p < .001) and their patients' longer sleep duration ( b = 0.61, p = .014), whereas patients' arousal and reactivity were associated with their caregivers' shorter SOL ( b = -8.47, p = .050). Patients' and caregivers' greater negative alterations in cognitions and mood were associated with patients' longer SOL ( b = 9.15, p = .014) and shorter sleep duration ( b = -0.41, p = .050), respectively. Caregivers' greater intrusion was related to their own shorter SOL ( b = -10.14, p = .004). CONCLUSIONS: The four PTSS clusters, particularly arousal and reactivity and negative cognitions and mood, have distinct associations with sleep markers individually and dyadically in patients and caregivers affected by cancer. Investigations of psychosocial and biobehavioral pathways underlying these relations are warranted. Tailored trauma treatments and sleep interventions may improve the well-being of this population.

27-year-old woman • postpartum seizures • PTSD • history of depression • Dx?

► Seizures with postpartum onset ► Posttraumatic stress disorder ► History of depression.

Recognizing risk and presence of posttraumatic stress disorder in women.

ABSTRACT: US women who report having experienced significant trauma at some point in their lives range from 50% to 90%. Yet posttraumatic stress disorder (PTSD) goes largely unrecognized in women. This article discusses ways to monitor, screen, and intervene for PTSD in women.

Moderating Effects of BDNF Genetic Variants and Smoking on Cognition in PTSD Veterans.

Posttraumatic stress disorder (PTSD) is frequently associated with cognitive disturbances and high prevalence of smoking. This study evaluated cognition in war veterans with PTSD and control subjects, controlled for the effect of smoking and brain derived neurotrophic factor (BDNF) rs6265 and rs56164415 genotypes/alleles. Study included 643 male war veterans with combat related PTSD and 120 healthy controls. Genotyping was done by real time PCR. Cognitive disturbances were evaluated using the Positive and Negative Syndrome Scale (PANSS) cognition subscale and the Rey-Osterrieth Complex Figure (ROCF) test scores. Diagnosis (p < 0.001), BDNF rs56164415 (p = 0.011) and smoking (p = 0.028) were significant predictors of the cognitive decline in subjects with PTSD. BDNF rs56164415 T alleles were more frequently found in subjects with PTSD, smokers and non-smokers, with impaired cognition, i.e., with the higher PANSS cognition subscale scores and with the lower ROCF immediate recall test scores. Presence of one or two BDNF rs56164415 T alleles was related to cognitive decline in PTSD. The T allele carriers with PTSD had advanced cognitive deterioration in smokers and nonsmokers with PTSD, and worse short-term visual memory function. Our findings emphasize the role of the BDNF rs56164415 T allele and smoking in cognitive dysfunction in war veterans with PTSD.

A Basomedial Amygdala to Intercalated Cells Microcircuit Expressing PACAP and Its Receptor PAC1 Regulates Contextual Fear.

Trauma can cause dysfunctional fear regulation leading some people to develop disorders, such as post-traumatic stress disorder (PTSD). The amygdala regulates fear, whereas PACAP (pituitary adenylate activating peptide) and PAC1 receptors are linked to PTSD symptom severity at genetic/epigenetic levels, with a strong link in females with PTSD. We discovered a PACAPergic projection from the basomedial amygdala (BMA) to the medial intercalated cells (mICCs) in adult mice. In vivo optogenetic stimulation of this pathway increased CFOS expression in mICCs, decreased fear recall, and increased fear extinction. Selective deletion of PAC1 receptors from the mICCs in females reduced fear acquisition, but enhanced fear generalization and reduced fear extinction in males. Optogenetic stimulation of the BMA-mICC PACAPergic pathway produced EPSCs in mICC neurons, which were enhanced by the PAC1 receptor antagonist, PACAP 6-38. Our findings show that mICCs modulate contextual fear in a dynamic and sex-dependent manner via a microcircuit containing the BMA and mICCs, and in a manner that was dependent on behavioral state.SIGNIFICANCE STATEMENT Traumatic stress can affect different aspects of fear behaviors, including fear learning, generalization of learned fear to novel contexts, how the fear of the original context is recalled, and how fear is reduced over time. While the amygdala has been studied for its role in regulation of different aspects of fear, the molecular circuitry of this structure is quite complex. In addition, aspects of fear can be modulated differently in males and females. Our findings show that a specific circuitry containing the neuropeptide PACAP and its receptor, PAC1, regulates various aspects of fear, including acquisition, generalization, recall, and extinction in a sexually dimorphic manner, characterizing a novel pathway that modulates traumatic fear.

Induced pluripotent stem cell-derived neural progenitor cell transplantation promotes regeneration and functional recovery after post-traumatic stress disorder in rats.

Post-traumatic stress disorder (PTSD) is a mental disorder characterized by hippocampal neuron loss and cognitive dysfunction. The aim of the present study was to investigate the potential functional outcomes of transplantation of induced pluripotent stem cell-derived neural progenitor cells (iPSC-NPCs) for treating PTSD. Human induced pluripotent stem cell (iPSCs), differentiated into neural progenitor cells (NPCs) in vitro, were transplanted into the brain of rat. Following iPSC-NPCs transplantation, cognitive function was determined. The open field test and fear condition test indicated that long-term iPSC-NPCs transplantation ameliorated cognitive dysfunction and reduced freezing time in PTSD rats. Following testing, the brain of rat was analyzed using immunocytochemistry and immunofluorescence. The results revealed that iPSC-NPCs differentiated into neurons replacing the loss of hippocampus neurons, and iPSC-NPCs transplantation showed higher expression of glial fibrillary acidic protein (GFAP) and increased number of NeuN compared with the control group. Moreover, western blot analysis suggested enhanced expression of brain-derived neurotrophic factor (BDNF) in hippocampus tissue of iPSC-NPCs transplanted rats in comparison to the PBS group. Collectively, these findings showed that iPSC-NPCs could promote regeneration and motor function recovery in PTSD model.

PI3K-Akt Signaling in the Basolateral Amygdala Facilitates Traumatic Stress Enhancements in Fear Memory.

BACKGROUND: A core symptom of posttraumatic stress disorder is persistent fear memory, which can be defined as fear memory that is resistant to updating, inhibition, or extinction. posttraumatic stress disorder emerges after traumatic stress exposure, but neurobiological mechanisms via which traumatic stress leads to persistent fear memory are not well defined. Akt signaling within the amygdala (Amy) is enhanced with traumatic stress, and phosphatidylinositol kinase 3 (PI3K) activation of Akt within the basolateral Amy (BLA) has been implicated as critical to fear memory formation. These findings raise the possibility that traumatic stress enhances PI3K→Akt signaling in the BLA, which leads to persistent fear memory. METHODS: To test this hypothesis, rats were exposed to traumatic stress using the single prolonged stress model, and changes in Akt phosphorylation were assayed in the Amy at 0 and 30 minutes after fear conditioning (FC). In a separate experiment, we inhibited PI3K→Akt signaling in the BLA prior to FC and observed the effect this had on acquisition, expression, and extinction of FC in stressed and control rats. RESULTS: Enhanced Akt phosphorylation in the Amy at both time points was observed in stressed rats, but not in control rats. PI3K→Akt inhibition in the BLA had no effect on freezing in control rats but decreased freezing during extinction training and testing in stressed rats. CONCLUSION: These findings suggest that PI3K→Akt signaling in the BLA could be a mechanism via which traumatic stress leads to fear memory that is resistant to extinction.

Phosphodiesterase-2 inhibitor reverses post-traumatic stress induced fear memory deficits and behavioral changes via cAMP/cGMP pathway.

Phosphodiesterase 2 is one of the phosphodiesterase (PDEs) family members that regulate cyclic nucleotide (namely cAMP and cGMP) concentrations. The present study determined whether PDE2 inhibition could rescue post-traumatic stress disorder (PTSD)-like symptoms. Mice were subjected to single prolonged stress (SPS) and treated with selective PDE2 inhibitor Bay 60-7550 (0.3, 1, or 3 mg/kg, i.p.). The behavioral tests such as forced swimming, sucrose preference test, open field, elevated plus maze, and contextual fear paradigm were conducted to determine the effects of Bay 60-7550 on SPS-induced depression- and anxiety-like behavior and fear memory deficits. The results suggested that Bay 60-7550 reversed SPS-induced depression- and anxiety-like behavior and fear memory deficits. Moreover, Bay 60-7550 prevented SPS-induced changes in the adrenal gland index, synaptic proteins synaptophysin and PSD95 expression, PKA, PKG, pCREB, and BDNF levels in the hippocampus and amygdala. These effects were completely prevented by PKG inhibitor KT5823. While PKA inhibitor H89 also prevented Bay 60-7550-induced pCREB and BDNF expression, but only partially prevented the effects on PSD95 expression in the hippocampus. These findings suggest that Bay 60-7550 protects mice against PTSD-like stress induced traumatic injury by activation of cGMP- or cAMP-related neuroprotective molecules, such as synaptic proteins, pCREB and BDNF.

Clinical Manifestations of Trauma Exposure in Fibromyalgia: The Role of Anxiety in the Association Between Posttraumatic Stress Symptoms and Fibromyalgia Status.

Little research has investigated how traumatic experiences relate to fibromyalgia (FM). We explored the presence of trauma exposure in a sample of Spanish participants with FM and examined the associations between (a) the number and type of traumatic experiences and posttraumatic stress disorder (PTSD) symptoms and (b) the severity of clinical manifestations in FM, testing for possible mediation models. Participants were 173 FM patients and 53 healthy controls aged 24 to 66 years. Traumatic event type (physical trauma, physical and sexual abuse, psychological trauma), PTSD symptoms, pain intensity, sleep disturbance, anxiety, depression, coping style, and daily functioning were evaluated via self-report. Fibromyalgia patients reported a higher percentage of trauma exposure than controls, more traumatic experiences (mainly emotional and physical trauma), and more PTSD symptoms, Hedges' gs/Cohen's ds = 0.42-0.76. Most FM patients reported having experienced their most distressing traumatic experience and PTSD symptoms before FM diagnosis. PTSD symptom severity was associated with more pain, sleep disturbances, anxiety, depression, coping style, and functional impairment, rs = .23-.33, ps = .025-.008. A multiple mediation analysis showed a significant indirect effect of anxiety in the association between PTSD symptoms and daily functioning. In a subset of FM patients, PTSD symptoms were associated with major clinical symptoms. The results suggest future research should explore the effectiveness of trauma-focused therapy compared to standard cognitive behavioral therapy for these patients.

Cumulative Risk on Oxytocin-Pathway Genes Impairs Default Mode Network Connectivity in Trauma-Exposed Youth.

Background: Although the default mode network (DMN) is a core network essential for brain functioning, little is known about its developmental trajectory, particularly on factors associated with its coherence into a functional network. In light of adult studies indicating DMN's susceptibility to stress-related conditions, we examined links between variability on oxytocin-pathway genes and DMN connectivity in youth exposed to chronic war-related trauma Methods: Following a cohort of war-exposed children from early childhood, we imaged the brains of 74 preadolescents (age 11-13 years; 39 war-exposed) during rest using magnetoencephalography (MEG). A cumulative risk index on oxytocin-pathway genes was constructed by combining single nucleotide polymorphisms on five genes previously linked with social deficits and psychopathology; OXTR rs1042778, OXTR rs2254298, OXTRrs53576, CD38 rs3796863, and AVPR1A RS3. Avoidant response to trauma reminders in early childhood and anxiety disorders in late childhood were assessed as predictors of disruptions to DMN theta connectivity. Results: Higher vulnerability on oxytocin-pathway genes predicted greater disruptions to DMN theta connectivity. Avoidant symptoms in early childhood and generalized anxiety disorder in later childhood were related to impaired DMN connectivity. In combination, stress exposure, oxytocin-pathway genes, and stress-related symptoms explained 24.6% of the variance in DMN connectivity, highlighting the significant effect of stress on the maturing brain. Conclusions: Findings are the first to link the oxytocin system and maturation of the DMN, a core system sustaining autobiographical memories, alteration of intrinsic and extrinsic attention, mentalization, and sense of self. Results suggest that oxytocin may buffer the effects of chronic early stress on the DMN, particularly theta rhythms that typify the developing brain.

Electroacupuncture ameliorates post-traumatic stress disorder in rats via a mechanism involving the BDNF-TrkB signaling pathway.

Post-traumatic stress disorder (PTSD) is a mental health condition triggered by a terrifying event, causing flashbacks, nightmares and severe anxiety. It develops in individuals who have experienced a shocking, scary, or dangerous event. Electroacupuncture is reported to be effective for the treatment of PTSD. The present study was carried out to investigate the protective effect of electroacupuncture in a rat model of PTSD, and the mechanism involved. Specific-pathogen-free male Sprague Dawley rats (n = 30) weighing 180 - 220 g (mean weight = 200 ± 20 g) were randomly assigned to three groups of ten rats each: control group, single-prolonged stress (SPS) group, and treatment group. The treatment group rats received electroacupuncture. Changes in PTSD-like behavior were assessed using locomotor activity, elevated plus-maze (EPM) and fear conditioning tests. The mRNA and protein expressions of brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) were determined using real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting, respectively. Co-immunoprecipitation (Co-IP) was used to measure BDNF and TrkB binding interaction, while chromatin immunoprecipitation (ChIP) was used to evaluate the binding between cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) and its target genes. Electroacupuncture significantly increased locomotor activity and exploratory behavior, but significantly reduced general fear and anxiety in SPS rats (p < 0.05). It also significantly upregulated the mRNA and protein expressions of BDNF and TrkB, and increased the binding of BDNF to its receptor TrkB (p < 0.05). Electroacupuncture significantly increased the binding of CREB to BDNF promoter region (p < 0.05). Electroacupuncture ameliorates PTSD in rats via a mechanism involving the BDNF-TrkB signaling pathway.

High IL-6 in military personnel relates to multiple traumatic brain injuries and post-traumatic stress disorder.

Repetitive traumatic brain injuries (TBIs) among military personnel have been linked to chronic behavioral and neurological symptoms, and poor health outcomes. Repetitive TBIs may impact inflammation, which may offer some explanation of the biological basis of these long-term risks, and may improve the care that is provided to these individuals. This study examines the concentrations of TNFα, IL-6 and IL-10 and associations with behavioral symptoms, including post-traumatic stress disorder symptoms and depression in a cohort of 106 military personnel and Veterans with a history of TBI. Group comparisons conducted for those with repetitive TBIs (> 3; n = 44), to participants with less than three TBIs (n = 29), and controls with no TBIs (n = 33). The primary outcomes were serum levels of inflammatory related proteins TNF-α, IL-6 and IL-10, TBI history, and PTSD symptoms. IL-6 mean concentration was significantly higher in the repetitive TBI group compared to those with 1-2 TBI or no TBI history (p = 0.050). Additionally, for participants with a history of TBI, PTSD symptom severity, specifically, intrusion (p = .006 and p = .007) and avoidance (p = .034 and .009), were significant predictors of higher IL-6 and IL-10 concentrations respectively. These findings suggest that repetitive TBIs concurrent with high PTSD symptoms in military personnel and Veterans are associated with chronic inflammation, and specifically elevated concentrations of IL-6. Examining the changes in inflammatory processes may identify potential therapeutic targets for early intervention after TBI in order to prevent the development of neurological deficits and disorders.

Case Series: Unilateral Amygdala Ablation Ameliorates Post-Traumatic Stress Disorder Symptoms and Biomarkers.

BACKGROUND: Post-traumatic stress disorder is a severe psychobiological disorder associated with hyperactivity of the amygdala, particularly on the right side. Highly selective laser ablation of the amygdalohippocampal complex is an effective neurosurgical treatment for medically refractory medial temporal lobe epilepsy that minimizes neurocognitive deficits relative to traditional open surgery. OBJECTIVE: To examine the impact of amygdalohippocampotomy upon symptoms and biomarkers of post-traumatic stress disorder. METHODS: Two patients with well-documented chronic post-traumatic stress disorder who subsequently developed late-onset epilepsy underwent unilateral laser amygdalohippocampotomy. Prospective clinical and neuropsychological measurements were collected in patient 1. Additional prospective measurements of symptoms and biomarkers were collected pre- and post-surgery in patient 2. RESULTS: After laser ablation targeting the nondominant (right) amygdala, both patients experienced not only reduced seizures, but also profoundly abated post-traumatic stress symptoms. Prospective evaluation of biomarkers in patient 2 showed robust improvements in hyperarousal symptoms, fear potentiation of the startle reflex, brain functional magnetic resonance imaging responses to fear-inducing stimuli, and emotional declarative memory. CONCLUSION: These observations support the emerging hypothesis that the right amygdala particularly perpetuates the signs and symptoms of post-traumatic stress disorder and suggests that focal unilateral amydalohippocampotomy can provide therapeutic benefit.

Individual susceptibility or resistance to posttraumatic stress disorder-like behaviours.

The aim of this study was to explore the neurobiological background of individual susceptibility and resistance to the development of posttraumatic stress disorder (PTSD)-like behaviours. Rats were divided into susceptible, PTSD(+), and resistant, PTSD(-), groups based on freezing duration during exposure to aversive context and the time spent in the central area in open field test one week after threefold stress experience (modified single prolonged stress). PTSD(-) rats showed increased concentrations of corticosterone in plasma and changes in GAD67 expression: decreased in the infralimbic cortex (IL) and increased in the lateral amygdala (LA), dentate gyrus (DG), and CA1 area of the hippocampus. Moreover, in this group, we found an increase in the number of CRF-positive nuclei in the parvocellular neurons of the paraventricular hypothalamic nucleus (pPVN). The PTSD(+) group, compared to PTSD(-) rats, had decreased concentrations of corticosterone in plasma and reduced CRF expression in the pPVN, higher CRF expression in the CA1, increased expression of CRF-positive nuclei and GR receptors in the CA3 area of the hippocampus, and increased expression of GR receptors in the DG and the central amygdala (CeA). Biochemical analysis showed higher concentrations of noradrenaline, glutamic acid in the dorsal hippocampus and amygdala and lower levels of dopamine and its metabolites in the amygdala of the PTSD(+) group than in the PTSD(-) group. The study revealed different behavioural and biochemical profiles of PTSD(+) and PTSD(-) rats and suggested that individual differences in hypothalamic-pituitary-adrenal (HPA) axis activity may determine hippocampal- and amygdala-dependent memory and fear processing.

Lower urinary symptoms, resilience, and post-traumatic stress symptoms among rectal cancer patients after surgery.

AIM: Disturbance of urinary function is a common complication after rectal cancer surgery, and it may affect patients' psychological well-being, consequently may develop post-traumatic stress disorder. Personal resilience might increase people's ability to manage life's challenges. However, limited study to explore their relationships. This study examined the relationships among lower urinary symptoms, resilience, and post-traumatic stress symptoms (PTSS) in post-surgery patients with rectal cancer. METHODS: A cross-sectional study design was used and included 188 patients with diagnosed rectal cancer who had undergone surgery over 24 months and were recruited from a hospital in southern Taiwan. The outcome measurements included a resilience scale, International Prostate Symptom Score (IPSS), the Chinese Davidson Trauma Scale, personal characteristics, and disease-related variables. RESULTS: There were significant relationships among age at diagnosed, self-reported physical status, perceived satisfied with recovery, urinary tract symptoms, resilience, and overall PTSS. The stepwise regression demonstrated that five factors, self-reported physical status, resilience, urinary tract symptoms, age at diagnosed and gender, and together explained 27.7% of overall PTSS variance (10.7, 6.7, 3.7, 4.8 and 1.8% of variance, respectively). CONCLUSION: The study demonstrates that patients with diagnosed rectal cancers long-term outcomes of PTSS, urinary tract symptoms, and resilience after surgery; in addition, self-reported physical status, resilience, urinary tract symptoms, age at diagnosed and gender are the major predictors of PTSS. A better understanding of the long-term outcomes of post-surgery in rectal cancer patients and its related factors may help to decreasing the PTSS after surviving cancer.

TLR4/MyD88/NF-κB-Mediated Inflammation Contributes to Cardiac Dysfunction in Rats of PTSD.

Post-traumatic stress disorder (PTSD) is related with myocardial injury and cardiac dysfunction, while the molecular mechanism has not been clear. This study investigated whether TLR4/MyD88/NF-κB-mediated inflammation involved in myocardial injury of PTSD. Adult male Wistar rats were exposed to single-prolonged stress (SPS), which was used broadly as a animal model of PTSD. Morris Water Maze (MWM) test and forced swimming test (FST) was carried out for behavioral testing. The protein expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the left ventricular of heart and TLR4/MyD88/NF-κB-mediated inflammation were examined. Our results showed that there were obvious increased in the protein expression of ANP and BNP in heart after exposure to SPS, SPS also significantly enhanced the serum level of IL-1ß and TNF-α, and meanwhile, the TLR4/MyD88/NF-κB pathway were activated. These results demonstrated that the TLR4/MyD88/NF-κB pathway were involved in the myocardial injury of PTSD, which might be one of possible molecular mechanism contributed to the pathogenesis of cardiac dysfunction in PTSD.

Stathmin Regulates Spatiotemporal Variation in the Memory Loop in Single-Prolonged Stress Rats.

Posttraumatic stress disorder (PTSD) is closely related to brain structures of the memory loop such as the hippocampus, amygdala, and medial prefrontal cortex (mPFC). The fear gene stathmin plays an important role in regulating fear memory. However, whether the fear gene stathmin is related to fear memory loop anomalies caused by PTSD is unclear. A single-prolonged stress (SPS) rat model of PTSD was constructed. Wistar rats were randomly divided into 5 groups: the control group, SPS 1-day group, SPS 4-day group, SPS 7-day group, and SPS 14-day group. Then, we measured the protein and mRNA expression of stathmin, p-stathmin (Ser16, Ser25, Ser38, and Ser63), ß-tubulin, and MAP-1B in the hippocampus, amygdala, and mPFC in the 5 groups by immunohistochemistry, Western blotting, and qRT-PCR. The expression of the stathmin protein in the hippocampus, mPFC, and amygdala of the rat memory loop decreased gradually in the SPS 1-day group, the SPS 4-day group, and the SPS 7-day group, in which it was the lowest, and then increased. The trend of the expression of stathmin mRNA in the three areas of the memory loop was consistent with the trend of the expression of the stathmin protein. The trend of the protein expression of p-stathmin (Ser25 and Ser38) was opposite of that of stathmin; it reached a peak on the 7th day, and then decreased in the hippocampus. The protein expression of p-stathmin (Ser63) showed the same trend in the mPFC. The protein and mRNA expression of ß-tubulin and MAP-1B was consistent with that of p-stathmin; it reached a peak on the 7th day, and then decreased in the rat hippocampus, mPFC, and amygdala. Stathmin in the memory loop, especially in the hippocampus, regulates microtubule structure through its phosphorylation at Ser25 and Ser38 and thereby participates in the mediation of fear memory abnormalities in PTSD.

The association between cognitive coping strategies and treatment outcomes in smokers with PTSD.

OBJECTIVE: Numerous researchers have suggested that certain coping styles (e.g., maladaptive cognitive coping strategies) interfere with recovery from traumatic experiences and contribute to the onset/maintenance of posttraumatic stress disorder (PTSD). Further, given that individuals with PTSD have a high rate of smoking (e.g., Mahaffey et al., 2016) and that maladaptive coping strategies in general are associated with lower smoking quit rates, it is possible that use of maladaptive cognitive coping strategies are particularly problematic for the recovery of smokers with PTSD. The present study examined whether specific cognitive coping strategies are associated with poorer outcome among smokers with PTSD following an integrated treatment for both disorders. METHOD: Patients with chronic PTSD and nicotine dependence (N = 142) received up to 12 sessions of smoking cessation counseling combined with varenicline or integrated prolonged exposure therapy and cessation counseling combined with varenicline. We hypothesized that greater maladaptive, and lower adaptive, cognitive coping strategies at baseline would moderate degree of improvement in smoking and PTSD outcomes through to follow-up. RESULTS: Multilevel modeling revealed that neither maladaptive nor adaptive cognitive coping strategies moderated smoking abstinence outcomes over the course of the study (ps ≥ .271). However, greater use of catastrophizing and lower use of positive reappraisal at baseline were associated with less improvement in the hyperarousal PTSD symptom cluster over the course of the study (ps ≤ .01). CONCLUSIONS: These findings suggest that maladaptive cognitive coping strategies are not necessarily a contraindication for overall outcomes in integrated PTSD and smoking treatment, although they may influence improvement in hyperarousal symptoms. (PsycINFO Database Record (c) 2020 APA, all rights reserved).