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Effects of Early Trauma on Psychosis Development in Clinical High-Risk Individuals and Stability of Trauma Assessment Across Studies: a Review Samantha L

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Effects of Early Trauma on Psychosis Development in Clinical High-Risk Individuals and Stability of Trauma Assessment Across Studies: a Review Samantha L Redman S.L. et al. Archives of Psychology, vol. 1, issue 3, December 2017 Page 1 of 23 RESEARCH ARTICLE Effects of early trauma on psychosis development in clinical high-risk individuals and stability of trauma assessment across studies: a review Samantha L. Redman1*, Cheryl M. Corcoran, David Kimhy, Dolores Malaspina2 Author Affiliations: Icahn School of Medicine at Mount Sinai, New York, New York, USA *Corresponding Author: Samantha Redman, Icahn School of Medicine at Mount Sinai, Department of Psychiatry, 53 E 96th Street, New York, NY 10128, phone: 212-659-8756, E-mail: [email protected] ____________________ 1 First Author 2 Senior Author Abstract: Early trauma (ET), though broadly and inconsistently defined, has been repeatedly linked to numerous psychological disturbances, including various developmental stages of psychotic disorders. The prodromal phase of psychosis highlights a unique and relevant population that provides insight into the critical periods of psychosis development. As such, a relatively recent research focus on individuals at clinical high risk (CHR) for psychosis reveals robust associations of early life trauma exposures with prodromal symptoms and function in these cohorts. While prevalence rates of ET in CHR cohorts remain consistently high, methodological measures of traumatic experiences vary across studies, presenting potential problems for reliability and validity of results. This review aims to 1) highlight the existing evidence identifying associations of ET, of multiple forms, with both symptom severity and transition rates to psychosis in CHR individuals, 2) present data on the variability among trauma assessments and its implications for conclusions about its relationship with clinical variables, 3) describe cognitive deficits common in CHR cohorts, including perceptual and neurocognitive impairments, and their neural correlates, that may modify the relationship of ET to symptoms, and 4) propose future directions for standardization of trauma assessment in CHR cohorts to better understand its clinical and cognitive correlates. Key Words: Early Trauma, Clinical High Risk, Psychosis, Trauma Assessment Introduction one‟s self or other that overwhelms one‟s ability to cope, frequently manifesting as Trauma, while relatively broad by fear, helplessness, or disorganized or interpretation, has been empirically defined agitated behavior (American Psychiatric as a highly stressful event that involves the Association, 2000). While more concrete threat of injury or threat to the integrity of uses of the word tend to reflect incidents of Copyright © 2017, Archives of Psychology. All rights reserved. http://www.archivesofpsychology.org Redman S.L. et al. Archives of Psychology, vol. 1, issue 3, December 2017 Page 2 of 23 physical threat, violation, or injury, as in the clinical patterns and phenomena observed in cases of sexual abuse, violence, or life- CHR populations, including attenuated threatening situations, the psychological psychotic symptoms, mood disturbances, experience of trauma is, by definition, and behavioral changes, offer a wealth of subjective. Thus, the individualized information for identifying potential risk experience and implications of trauma vary factors that may enhance early intervention by many factors, including a wide range of and possible prevention efforts. The CHR biological and environmental features. paradigm has gained considerable attention Along the spectrum of traumatic life in recent years due to accumulating evidence experiences, early trauma (ET) in childhood that demonstrates its clinical importance, and adolescence has been consistently linked and this paradigm provides researchers with to psychosis in adulthood (Read, van Os, a unique window into a critical Morrison, & Ross, 2005; Spauwen, developmental period in psychotic disorders. Krabbendam, Lieb, Wittchen, & van Os, 2006). Recent literature has considered Investigators have long debated the childhood trauma exposure as a potential respective roles of genetic and precipitator in the pathogenesis of psychosis environmental factors in the etiology of (Falukozi & Addington, 2012; Arseneault et psychosis, though the current consensus al., 2011; Tikka et al., 2013) and as a factor emphasizes a synergistic relationship that shapes the clinical features of the illness between the two. Aside from biological (Ruby et al., 2014; Veras et al., 2017; vulnerability, several socio-environmental Bechdolf et al., 2010; Thompson et al., factors have been found to increase risk for 2010; Thompson et al., 2011). psychosis (Van Winkel, Stefanis, & Myin- Germeys, 2008). Among them, ET is most The “clinical high risk” (CHR) model for consistently linked to negative physical and psychosis risk underscores a series of mental health outcomes later in life genetic and environmental risks factors that (Ashcroft, Kingdon & Chadwick, 2012). are associated with an increased While ET has been studied extensively in vulnerability for developing psychosis relation to psychotic symptoms, the (McGorry, Yung, & Phillips, 2003). specificity of this relationship, especially in Alternatively referred to as the ultra-high- CHR populations, remains unclear. risk (UHR) state for psychosis, inclusion criteria for this population is defined by This review focuses on the extant literature three non-exclusive, internationally on the associations of early exposure to validated conditions: (1) attenuated trauma with symptoms in CHR cohorts. We psychotic symptoms (APS), (2) brief and begin by reporting on the existing evidence limited intermittent psychotic symptoms that identifies ET, of multiple varieties, as a (BLIPS), and (3) genetic risk and consistent component of the CHR profile, deterioration syndrome (GRD) (Fusar-Poli et and its potential relationship to transition al., 2015). The initial concept of the rates to psychosis. We then describe the prodromal state was defined clinically as a methodologies of these studies in respect to period of distress and disturbance that different trauma assessments, outlining the precedes the first psychotic episode, often strengths and weaknesses of different experienced in early teen and young adult assessments, and the ramifications for years (Yung & McGorry, 1996). While the drawing clear conclusions about the majority (approximately 65%) of those relationship of trauma to symptoms. Next, labeled as CHR do not transition to we discuss distinguishable patterns of psychosis (Mayo et al., 2017), a range of trauma type among CHR cohorts and examine the neurobiological, perceptual, and Copyright © 2017, Archives of Psychology. All rights reserved. http://www.archivesofpsychology.org Redman S.L. et al. Archives of Psychology, vol. 1, issue 3, December 2017 Page 3 of 23 neurocognitive impairments in CHR positive symptoms and ET in their CHR individuals that may confound or modify cohort and Kline et al. (2016) linked ET these associations. Finally, we discuss future broadly to positive symptoms in CHR and research directions in respect to early-psychosis groups. Earlier studies standardization of trauma assessment across explored the association between specific CHR cohorts, and its implication for positive symptoms and various types of understanding mental health outcomes of trauma exposure, finding significant CHR individuals. correlations of childhood trauma with both hallucinations and delusions (Read, van Os, 1. Effects of Trauma on Symptom Morrison, & Ross, 2005). Victims of early Specificity sexual and physical abuse exhibit significantly more positive symptoms, Up to 90% of individuals at CHR for including voices commenting, ideas of psychosis report a lifetime history of reference, thought insertion, paranoid traumatic events and victimization in ideation, mind-reading, and visual childhood (Mayo et al., 2017). When hallucinations, as compared to individuals compared to non-psychiatric controls, CHR with no abuse history (Ross, Anderson, & individuals endorse much higher rates of Clark, 1994). Increased ET has been traumatic events, with a mean prevalence significantly correlated with delusional rate of approximately 85% across CHR thinking, including grandiose thoughts of samples (Addington et al., 2013; Kraan, status and power, feelings of being watched Velthorst, Smit, Haan, & van der Gaag, or followed, and unusual negative thoughts 2015). CHR individuals with trauma regarding the self (Falukozi & Addington, histories exhibit significantly higher 2012). Positive symptoms are strongly transition rates to psychosis than those with linked to increased dopaminergic no reported trauma exposure (Bechdolf et transmission, while early trauma and stress al., 2010). A meta-analysis of studies on can elicit elevated glucocorticoid levels trauma in CHR cohorts reveals that (Ruby et al., 2014). Given the interaction childhood adversity/ET has an estimated between glucocorticoid and dopaminergic 33% attributable risk for psychosis, even pathways, the mechanisms underlying this after controlling for potential confounds association may be that early experiences of such as genetic vulnerability, comorbidities, trauma increase glucocorticoid levels, drug use, ethnicity, urbanicity, and IQ subsequently leading to hyperactivity of (Varese et al., 2012). These data indicate a dopaminergic systems, and ultimately the clear relationship between traumatic events development of positive symptoms in in childhood and risk for psychosis. We adolescence and young adulthood. build on these findings by looking at associations
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