Giving Voice to Silence: Empowerment and Disempowerment in the Developmental Shift from Trauma ‘Victim’ to ‘Survivor-Advocate’

ABSTRACT

In the past several years, a public conversation in the United States about interpersonal violence has flourished, sustained by the work of advocates who are themselves survivors. This surge in public sharing of trauma stories is a rhetorical form of resistance to ideologies in mainstream American culture that impose silence on survivors (e.g., the “just world” belief). However, the developmental progression from trauma ‘victim’ to empowered public ‘survivor/advocate’ accommodates to dominant American cultural preferences that stories of adversity have a redemptive story line. In a redemptive story, negative experiences are followed by something positive (e.g., personal growth, lessons learned, strength gained). In this paper, we draw from theory and the sparse relevant literature across multiple disciplines to conceptualize when and for whom the redemptive storying of trauma (or, redemptive master narrative) is available, advantageous, and systemically encouraged. Among the proposed advantages of redemptive storying are its psychological health benefits; potential to empower self and others; promotion of meaning-making, mission, and communal solidarity; and the larger social/political changes that can emerge from giving voice to silenced experiences. Proposed challenges to redemptive storying include layers of societal oppression and marginalization that shape the redemption stories of many survivor-advocates; ongoing connection to or dependence on relationships and communities that enable abuse; and the reality of historical trauma and other forms of intergenerational trauma, which complicate the linear, individualistic story of redemption. With this theory-driven framework, we wish to promote compassion for survivors, along with interdisciplinary, inclusive, and intersectional research in this understudied area.     

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

BackgroundA 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.MethodsTo 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.ResultsEnhanced 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.ConclusionThese 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.     

Side by Side Treadmill Walking With Intentionally Desynchronized Gait

Humans demonstrate an innate desire to synchronize stepping when walking side by side. This behavior requires modification of each person’s gait, which may increase for pairings with very different walking patterns. The purpose of this study was to compare locomotor behavior for conditions in which partners exhibited similar and substantially different walking patterns. Twenty-six unimpaired subjects walked on a motorized treadmill at their preferred walking speed for three trials: by themselves (SOLO), next to someone on an adjacent treadmill (PAIRED), and next to someone who purposely avoided synchronization by altering stride times and/or lengths (DeSYNC). Means, coefficients of variance, approximate entropy (ApEn), rate of autocorrelation decay (α), and estimates of maximal Lyapunov exponents (λ*) were calculated for several dependent variables taken from sagittal plane kinematic data. Few differences in behavior were noted when the PAIRED condition was compared to the SOLO condition. However, the DeSYNC condition resulted in several alterations in ApEn, α, and λ*. These results suggest that greater differences in walking pattern between partners will facilitate greater modification to an individual’s gait. Additional study of side by side walking may hold implications for understanding the control of gait in humans and may have application in a clinical setting.     

Bitemporal Scalp Hair Loss: Differential Diagnosis of Nonscarring and Scarring Conditions

BACKGROUND: Bitemporal hair loss can be a diagnostic challenge because several entities may affect this region of the scalp, including both scarring and nonscarring conditions. Although traction alopecia is the most common cause of bitemporal hair loss, no studies to date have outlined all of the potential causes. OBJECTIVE: We sought to review nonscarring and scarring conditions that have a clinical presentation of bitemporal hair loss, including traction alopecia, telogen effluvium, female pattern hair loss, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, and seborrheic dermatitis. METHODS: A Google Scholar and PubMed literature search were conducted for this review. The keywords used in the search included the following: “traction alopecia”, “telogen effluvium”, “androgenic alopecia”, “androgenetic alopecia”, “female pattern hair loss”, “alopecia areata”, “frontal fibrosing alopecia”, “central centrifugal cicatricial alopecia”, and “seborrheic dermatitis”. The scope of our search included all research articles published from 1957 to February 2019. In total, 94 articles regarding non-scarring and scarring hair loss were selected and included according to topic relevance. Exclusion criteria included articles that did not address the epidemiology and/or clinicopathologic or dermatoscopic findings of non-scarring and scarring forms of alopecia. Inclusion criteria included articles that addressed a clinical presentation of bitemporal hair loss; or addressed epidemiology, clinical presentation, dermatoscopic findings, and/or treatment. RESULTS: Bitemporal hair loss is a common and often distressing condition with a broad differential. CONCLUSION: Clinicians must be aware of the potential causes of bitemporal hair loss. Prompt diagnosis is essential to prevent further hair loss, especially in scarring conditions.     

Inhaled CD86 antisense oligonucleotide suppresses pulmonary inflammation and airway hyper-responsiveness in allergic mice

The B7-family molecule CD86, expressed on the surface of pulmonary and thoracic lymph node antigen-presenting cells, delivers essential costimulatory signals for T-cell activation in response to inhaled allergens. CD86-CD28 signaling is involved in priming allergen-specific T cells, but it is unclear whether these interactions play a role in coordinating memory T-helper 2 cell responses. In the ovalbumin (OVA)-induced mouse model of asthma, administration of CD86-specific antibody before systemic sensitization suppresses inhaled OVA-induced pulmonary inflammation and airway hyper-responsiveness (AHR). In previously OVA-sensitized mice, systemic and intranasal coadministration of CD86 antibody is required to produce these effects. To directly assess the importance of pulmonary CD86 expression in secondary immune responses to inhaled allergens, mice were sensitized and locally challenged with nebulized OVA before treatment with an inhaled aerosolized CD86 antisense oligonucleotide (ASO). CD86 ASO treatment suppressed OVA-induced up-regulation of CD86 protein expression on pulmonary dendritic cells and macrophages as well as on recruited eosinophils. Suppression of CD86 protein expression correlated with decreased methacholine-induced AHR, airway inflammation, and mucus production following rechallenge with inhaled OVA. CD86 ASO treatment reduced BAL eotaxin levels, but it did not reduce CD86 protein on cells in the draining lymph nodes of the lung, and it had no effect on serum IgE levels, suggesting a local and not a systemic effect. These results demonstrate that CD86 expression on pulmonary antigen-presenting cells plays a vital role in regulating pulmonary secondary immune responses and suggest that treatment with an inhaled CD86 ASO may have utility in asthma and other chronic inflammatory lung conditions.     

Evidence for phase-based psychotherapy as a treatment for dissociative identity disorder comorbid with major depressive disorder and alcohol dependence

We report on the treatment and successful outcome of a 58-year-old Native American male with a history of complex trauma presenting with dissociative identity disorder (DID) and major depressive disorder. The treatment included a trauma-informed phase-based psychotherapy as recommended by the International Society for the Study of Trauma and Dissociation for treating DID. We assessed symptoms at baseline and at three additional time points over the course of 14 months. We utilized the Reliable Change Index to examine statistically significant change in symptoms over the course of treatment. Significant symptom improvements were realized posttreatment across all measured domains of functioning, including dissociative symptoms, alcohol abuse, depression, anxiety, and emotion regulation skills. Moreover, the client no longer met criteria for DID, major depressive disorder, or alcohol abuse. Results are discussed in terms of the effectiveness of trauma-focused, phase-based treatment for DID for cases of complex trauma with comorbid disorders.