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      • Record: found
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      Substance use, childhood traumatic experience, and Posttraumatic Stress Disorder in an urban civilian population.

      Author(s): 1 , , , ,  
      Publication date (Electronic):
      Journal: Depression and anxiety
      Publisher: Wiley

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          Abstract

          Exposure to traumatic experiences, especially those occurring in childhood, has been linked to substance use disorders (SUDs), including abuse and dependence. SUDs are also highly comorbid with Posttraumatic Stress Disorder (PTSD) and other mood-related psychopathology. Most studies examining the relationship between PTSD and SUDs have examined veteran populations or patients in substance treatment programs. The present study further examines this relationship between childhood trauma, substance use, and PTSD in a sample of urban primary care patients.

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          Reliability and validity of a brief instrument for assessing post-traumatic stress disorder

          Edna B. Foa, David S. Riggs, Constance Dancu … (1993)
          Article 0 comments Cited 379 times – based on 0 reviews     Review now
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            Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.

            Elisabeth B Binder, Rebekah G Bradley, Wei. Liu … (2008)
            In addition to trauma exposure, other factors contribute to risk for development of posttraumatic stress disorder (PTSD) in adulthood. Both genetic and environmental factors are contributory, with child abuse providing significant risk liability. To increase understanding of genetic and environmental risk factors as well as their interaction in the development of PTSD by gene x environment interactions of child abuse, level of non-child abuse trauma exposure, and genetic polymorphisms at the stress-related gene FKBP5. A cross-sectional study examining genetic and psychological risk factors in 900 nonpsychiatric clinic patients (762 included for all genotype studies) with significant levels of childhood abuse as well as non-child abuse trauma using a verbally presented survey combined with single-nucleotide polymorphism (SNP) genotyping. Participants were primarily urban, low-income, black (>95%) men and women seeking care in the general medical care and obstetrics-gynecology clinics of an urban public hospital in Atlanta, Georgia, between 2005 and 2007. Severity of adult PTSD symptomatology, measured with the modified PTSD Symptom Scale, non-child abuse (primarily adult) trauma exposure and child abuse measured using the traumatic events inventory and 8 SNPs spanning the FKBP5 locus. Level of child abuse and non-child abuse trauma each separately predicted level of adult PTSD symptomatology (mean [SD], PTSD Symptom Scale for no child abuse, 8.03 [10.48] vs > or =2 types of abuse, 20.93 [14.32]; and for no non-child abuse trauma, 3.58 [6.27] vs > or =4 types, 16.74 [12.90]; P < .001). Although FKBP5 SNPs did not directly predict PTSD symptom outcome or interact with level of non-child abuse trauma to predict PTSD symptom severity, 4 SNPs in the FKBP5 locus significantly interacted (rs9296158, rs3800373, rs1360780, and rs9470080; minimum P = .0004) with the severity of child abuse to predict level of adult PTSD symptoms after correcting for multiple testing. This gene x environment interaction remained significant when controlling for depression severity scores, age, sex, levels of non-child abuse trauma exposure, and genetic ancestry. This genetic interaction was also paralleled by FKBP5 genotype-dependent and PTSD-dependent effects on glucocorticoid receptor sensitivity, measured by the dexamethasone suppression test. Four SNPs of the FKBP5 gene interacted with severity of child abuse as a predictor of adult PTSD symptoms. There were no main effects of the SNPs on PTSD symptoms and no significant genetic interactions with level of non-child abuse trauma as predictor of adult PTSD symptoms, suggesting a potential gene-childhood environment interaction for adult PTSD.
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              Comparison of the PTSD symptom scale-interview version and the clinician-administered PTSD scale

              Edna B. Foa, David F Tolin (2000)
              The Clinician-Administered PTSD Scale (CAPS) is one of the most frequently used measures of posttraumatic stress disorder (PTSD). It has been shown to be a reliable and valid measure, although its psychometric properties in nonveteran populations are not well known. One problem with the CAPS is its long assessment time. The PTSD Symptom Scale--Interview Version (PSS-I) is an alternative measure of PTSD severity, requiring less assessment time than the CAPS. Preliminary studies indicate that the PSS-I is reliable and valid in civilian trauma survivors. In the present study we compared the psychometric properties of the CAPS and the PSS-I in a sample of 64 civilian trauma survivors with and without PTSD. Participants were administered the CAPS, the PSS-I, and the Structured Clinical Interview for DSM-IV (SCID) by separate interviewers, and their responses were videotaped and rated by independent clinicians. Results indicated that the CAPS and the PSS-I showed high internal consistency, with no differences between the two measures. Interrater reliability was also high for both measures, with the PSS-I yielding a slightly higher coefficient. The CAPS and the PSS-I correlated strongly with each other and with the SCID. Although the CAPS had slightly higher specificity and the PSS-I had slightly higher sensitivity to PTSD, overall the CAPS and the PSS-I performed about equally well. These results suggest that the PSS-I can be used instead of the CAPS in the assessment of PTSD, thus decreasing assessment time without sacrificing reliability or validity.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Depress Anxiety
                Title: Depression and anxiety
                Publisher: Wiley
                ISSN (Electronic): 1520-6394
                ISSN (Print): 1091-4269
                Publication date (Electronic): Dec 2010
                Volume: 27
                Issue: 12
                Affiliations
                [1 ] Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia 30329, USA.
                Article
                Mid ID: NIHMS231214
                DOI: 10.1002/da.20751
                PMC ID: 3051362
                PubMed ID: 21049532
                SO-VID: 47f76c4d-fdde-4347-b440-24e72c4c29c0
                Copyright © © 2010 Wiley-Liss, Inc.
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