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1.
Psychoneuroendocrinology ; 51: 589-97, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25212409

RESUMO

BACKGROUND: Prolonged exposure (PE) therapy for post-traumatic stress disorder (PTSD) in military veterans has established efficacy, but is ineffective for a substantial number of patients. PE is also associated with high dropout rates. We hypothesized that hydrocortisone augmentation would enhance symptom improvement and reduce drop-out rates by diminishing the distressing effects of traumatic memories retrieved during imaginal exposure. We also hypothesized that in responders, hydrocortisone augmentation would be more effective in reversing glucocorticoid indices associated with PTSD than placebo augmentation. METHOD: Twenty-four veterans were randomized to receive either 30 mg oral hydrocortisone or placebo prior to PE sessions 3-10 in a double-blind protocol. Glucocorticoid receptor sensitivity was assessed in cultured peripheral blood mononuclear cells (PBMC) using the in vitro lysozyme inhibition test and was determined before and after treatment. Intent-to-treat analysis was performed using latent growth curve modeling of treatment effects on change in PTSD severity over time. Veterans who no longer met diagnostic criteria for PTSD at post-treatment were designated as responders. RESULTS: Veterans randomized to hydrocortisone or placebo augmentation did not differ significantly in clinical severity or glucocorticoid sensitivity at pre-treatment. Hydrocortisone augmentation was associated with greater reduction in total PTSD symptoms compared to placebo, a finding that was explained by significantly greater patient retention in the hydrocortisone augmentation condition. A significant treatment condition by responder status interaction for glucocorticoid sensitivity indicated that responders to hydrocortisone augmentation had the highest pre-treatment glucocorticoid sensitivity (lowest lysozyme IC50-DEX) that diminished over the course of treatment. There was a significant association between decline in glucocorticoid responsiveness and improvement in PTSD symptoms among hydrocortisone recipients. CONCLUSIONS: The results of this pilot study suggest that hydrocortisone augmentation of PE may result in greater retention in treatment and thereby promote PTSD symptom improvement. Further, the results suggest that particularly elevated glucocorticoid responsiveness at pre-treatment may identify veterans likely to respond to PE combined with an intervention that targets glucocorticoid sensitivity. Confirmation of these findings will suggest that pharmacologic interventions that target PTSD-associated glucocorticoid dysregulation may be particularly helpful in promoting a positive clinical response to PTSD psychotherapy.


Assuntos
Hidrocortisona/uso terapêutico , Terapia Implosiva/métodos , Transtornos de Estresse Pós-Traumáticos/terapia , Adulto , Idoso , Terapia Combinada , Método Duplo-Cego , Humanos , Masculino , Pessoa de Meia-Idade , Militares , Projetos Piloto , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/psicologia , Resultado do Tratamento
2.
Interface Focus ; 4(5): 20140048, 2014 Oct 06.
Artigo em Inglês | MEDLINE | ID: mdl-25285201

RESUMO

The identification of biomarkers for post-traumatic stress disorder (PTSD) and resilience/recovery is critical for advancing knowledge about pathophysiology and treatment in trauma-exposed persons. This study examined a series of glucocorticoid-related biomarkers prior to and in response to psychotherapy. Fifty-two male and female veterans with PTSD were randomized 2 : 1 to receive either prolonged exposure (PE) therapy or a weekly minimal attention (MA) intervention for 12 consecutive weeks. Psychological and biological assessments were obtained prior to and following treatment and after a 12-week naturalistic follow-up. Response was defined dichotomously as no longer meeting criteria for PTSD at post-treatment based on the Clinician Administered PTSD Scale for DSM-IV (CAPS). Clinical improvement on the CAPS was apparent for both PE and MA, with no significant difference according to treatment condition. Biomarkers predictive of treatment gains included the BCLI polymorphism of the glucocorticoid receptor gene. Additional predictors of treatment response were higher bedtime salivary cortisol and 24 h urinary cortisol excretion. Pre-treatment plasma dehydroepiandrosterone/cortisol ratio and neuropetide Y (NPY) levels were predictors of reductions in PTSD symptoms, and, for NPY only, of other secondary outcomes as well, including anxiety and depression ratings. Glucocorticoid sensitivity changed in association with symptom change, reflecting clinical state. It is possible to distinguish prognostic and state biomarkers of PTSD using a longitudinal approach in the context of treatment. Identified markers may also be relevant to understanding mechanisms of action of symptom reduction.

3.
Psychoneuroendocrinology ; 40: 213-20, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24485493

RESUMO

Intergenerational effects of trauma have been observed clinically in a wide range of populations, and parental PTSD has been associated with an increased risk for psychopathology in offspring. In studies of Holocaust survivor offspring, parental PTSD, and particularly maternal PTSD, has been associated with increased risk for PTSD, low basal urinary cortisol excretion and enhanced cortisol suppression in response to dexamethasone. Such findings implicate maternally derived glucocorticoid programming in the intergenerational transmission of trauma-related consequences, potentially resulting from in utero influences or early life experiences. This study investigated the relative influence of Holocaust exposure and PTSD in mothers and fathers on glucocorticoid sensitivity in offspring. Eighty Holocaust offspring and 15 offspring of non-exposed Jewish parents completed evaluations and provided blood and urine samples. Glucocorticoid sensitivity was evaluated using the lysozyme suppression test (LST), an in vitro measure of glucocorticoid receptor sensitivity in a peripheral tissue, the dexamethasone suppression test (DST), and 24-h urinary cortisol excretion. Maternal PTSD was associated with greater glucocorticoid sensitivity in offspring across all three measures of glucocorticoid function. An interaction of maternal and paternal PTSD on the DST and 24-h urinary cortisol showed an effect of decreased glucocorticoid sensitivity in offspring with paternal, but not maternal, PTSD. Although indirect, these findings are consistent with the hypothesis that epigenetic programming may be involved in the intergenerational transmission of trauma-related effects on glucocorticoid regulation.


Assuntos
Filho de Pais com Deficiência , Glucocorticoides/metabolismo , Holocausto , Mães/psicologia , Efeitos Tardios da Exposição Pré-Natal/psicologia , Transtornos de Estresse Pós-Traumáticos , Sobreviventes , Adulto , Idoso , Transtornos de Ansiedade/sangue , Transtornos de Ansiedade/epidemiologia , Transtornos de Ansiedade/etiologia , Transtornos de Ansiedade/urina , Estudos de Casos e Controles , Transtorno Depressivo/sangue , Transtorno Depressivo/epidemiologia , Transtorno Depressivo/etiologia , Transtorno Depressivo/urina , Pai/psicologia , Pai/estatística & dados numéricos , Feminino , Holocausto/psicologia , Humanos , Hidrocortisona/sangue , Hidrocortisona/urina , Masculino , Pessoa de Meia-Idade , Mães/estatística & dados numéricos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Sobreviventes/psicologia , Sobreviventes/estatística & dados numéricos , Adulto Jovem
4.
Expert Opin Pharmacother ; 12(15): 2339-54, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21819273

RESUMO

INTRODUCTION: Posttraumatic stress disorder (PTSD) is a complex disorder associated with an intricate biological and psychological symptom profile and various common comorbidities. Despite an existing myriad of evidence-based and experimental treatments, PTSD is often difficult to treat. This reality necessitates a discussion of the potential of emerging treatments. AREAS COVERED: A literature search using PubMed and PsychInfo was done using the following keywords: randomized clinical trials, treatment guidelines, pharmacotherapy and psychotherapy, all in addition to PTSD. A comprehensive treatment review establishes that early intervention approaches have not yet been found to prevent PTSD in trauma survivors. However, psychotherapy research provides substantial support for cognitive behavioral therapies and eye movement desensitization and reprocessing for chronic PTSD, and psychopharmacological approaches are myriad - although at present there is FDA approval only for sertraline and paroxetine. However, the efficacy of these treatments varies and, unfortunately, not everyone will achieve remission. EXPERT OPINION: So far, the mental health field has tended to focus on either biological or psychological targets. We propose that maximizing treatment success may require an integrated approach that does not dichotomize biological and psychological aspects. Exciting new developments reflecting this perspective include psychopharmacologic augmentation strategies that enhance the mechanisms of psychotherapy.


Assuntos
Terapia Cognitivo-Comportamental , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/terapia , Terapia Combinada , Dessensibilização e Reprocessamento através dos Movimentos Oculares , Humanos , Inibidores Seletivos de Recaptação de Serotonina/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/psicologia
5.
Dev Psychopathol ; 23(2): 477-91, 2011 May.
Artigo em Inglês | MEDLINE | ID: mdl-23786690

RESUMO

The effects of childhood abuse are diverse, and although pathology is not the only outcome, psychiatric illness, including posttraumatic stress disorder (PTSD), can develop. However, adult PTSD is less common among those who experienced single-event traumas as children than it is among those who experienced childhood abuse. In addition, PTSD is more common among adults than children who experienced childhood abuse. Such evidence raises doubt about the direct, causal link between childhood trauma and adult PTSD. The experience of childhood trauma, and in particular abuse, has been identified as a risk factor for subsequent development of PTSD following exposure to adult trauma, and a substantial literature identifies revictimization as a factor that plays a pivotal role in this trajectory. The literature on the developmental effects of childhood abuse and pathways to revictimization, when considered in tandem with the biological effects of early stress in animal models, may provide some explanations for this. Specifically, it seems possible that permanent sensitization of the hypothalamic-pituitary-adrenal axis and behavioral outcomes are a consequence of childhood abuse, and these combine with the impact of retraumatization to sustain, perpetuate, and amplify symptomatology of those exposed to maltreatment in childhood.


Assuntos
Maus-Tratos Infantis/psicologia , Transtornos de Estresse Pós-Traumáticos/etiologia , Criança , Humanos , Sistema Hipotálamo-Hipofisário/fisiopatologia , Acontecimentos que Mudam a Vida , Sistema Hipófise-Suprarrenal/fisiopatologia , Fatores de Risco , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Transtornos de Estresse Pós-Traumáticos/psicologia
6.
Ann N Y Acad Sci ; 1208: 158-63, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20955338

RESUMO

Combat veterans with posttraumatic stress disorder (PTSD) demonstrate less robust improvement following treatments than do civilians with PTSD. This paper discusses a theoretical model for evaluating treatment response based on the extent of change in biological markers of symptom severity or resilience between treatment initiation and termination. Such analysis permits a determination of biological change associated with the liberal criteria commonly used to determine treatment response in combat PTSD, and a comparison of this to the biological change associated with clinical response determined according to the conservative definition more appropriate to civilian PTSD. Interim data supporting the utility of this approach is presented based on preliminary analyses from our work in progress. We propose that future studies consider the unique consequences of combat trauma and develop treatments that incorporate the complex nature of the exposure and response characteristic of a veteran population.


Assuntos
Biomarcadores/metabolismo , Transtornos de Estresse Pós-Traumáticos/metabolismo , Transtornos de Estresse Pós-Traumáticos/terapia , Desidroepiandrosterona/metabolismo , Humanos , Terapia Implosiva , Receptores de Glucocorticoides/metabolismo , Transtornos de Estresse Pós-Traumáticos/psicologia , Resultado do Tratamento , Veteranos/psicologia
7.
Psychiatry Res ; 184(2): 117-27, 2010 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-20934312

RESUMO

Neuroendocrine, cognitive and hippocampal alterations have been described in Gulf War (GW) veterans, but their inter-relationships and significance for posttraumatic stress disorder (PTSD) have not been described. Hydrocortisone (Hcort) was administered to GW veterans with (PTSD+ n=12) and without (PTSD- n=8) chronic PTSD in a randomized, placebo-controlled, double-blind challenge. Changes in plasma ACTH, memory, and hippocampal [(18)F]FDG uptake on positron emission tomography were assessed. The low-dose dexamethasone suppression test was also administered. The PTSD+ group showed greater cortisol and ACTH suppression, reflecting greater peripheral glucocorticoid receptor (GR) responsiveness, and did not show an Hcort-induced decrement in delayed recall or retention. The groups had comparable relative regional hippocampal [(18)F]FDG uptake at baseline, but only the PTSD- group had an Hcort-associated decrease in hippocampal [(18)F]FDG uptake. Asymmetry in hippocampal hemispheric volumes differed between PTSD+ and PTSD- groups. This asymmetry was associated with cortisol, ACTH, retention and functional hippocampal asymmetry before, but not after, Hcort administration. Differences in brain metabolic responses between GW veterans with and without PTSD may reflect differences in peripheral and central GR responsiveness.


Assuntos
Hormônio Adrenocorticotrópico/sangue , Hipocampo/efeitos dos fármacos , Hidrocortisona/administração & dosagem , Memória/efeitos dos fármacos , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Veteranos , Adulto , Análise de Variância , Método Duplo-Cego , Ensaio de Imunoadsorção Enzimática , Guerra do Golfo , Hipocampo/diagnóstico por imagem , Hipocampo/metabolismo , Humanos , Hidrocortisona/sangue , Processamento de Imagem Assistida por Computador , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos , Cintilografia , Transtornos de Estresse Pós-Traumáticos/diagnóstico por imagem , Transtornos de Estresse Pós-Traumáticos/metabolismo
8.
Psychopharmacology (Berl) ; 212(3): 405-17, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20706708

RESUMO

RATIONALE: Early Life Stress (ELS) increases risk for both adult traumatization and posttraumatic stress disorder (PTSD). Adult PTSD may also reflect a continuation of a response to an earlier exposure to adversity. Given similarities between neuroendocrine aspects of PTSD and ELS, such as in reduced cortisol signaling and glucocorticoid receptor (GR) responsiveness, some aspects of the biology of PTSD may reflect biological correlates of risk. OBJECTIVES: This paper will examine how empirical findings regarding the biological basis of ELS can inform our understanding of the neuroendocrinology of PTSD. This paper will also propose a hypothetical model to guide future research that integrates genetic, epigenetic, neuroendocrine, and psychological observations to understand the contribution of ELS neurobiology to PTSD. RESULTS: Recent genetic findings demonstrate heritable aspects of at least some of these cortisol-related disturbances. Furthermore, ELS may produce at least some of the PTSD-associated changes in glucocorticoid responsiveness through epigenetic mechanisms such as developmental programming. These, then, may contribute to enduring changes in stress responsiveness as well as enhanced risk for adult exposure and PTSD. CONCLUSION: Molecular mechanisms associated with gene x environment interactions or GR programming are essential in explaining current observations in the neuroendocrinology of PTSD that have been difficult to understand through the lens of contemporary stress theory.


Assuntos
Modelos Psicológicos , Transtornos de Estresse Pós-Traumáticos/etiologia , Estresse Psicológico/complicações , Adulto , Animais , Criança , Epigênese Genética , Predisposição Genética para Doença , Humanos , Hidrocortisona/metabolismo , Receptores de Glucocorticoides/metabolismo , Fatores de Risco , Transtornos de Estresse Pós-Traumáticos/genética , Transtornos de Estresse Pós-Traumáticos/psicologia
9.
Psychiatr Clin North Am ; 33(2): 465-74, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-20385347

RESUMO

Posttraumatic stress disorder (PTSD) as a response to trauma is repeatedly found to be more common among women than men. This article explores prevalence rates and gender differences. Explanations for this gender bias and examined and the literature on trauma types and resulting PTSD is reviewed. Other disorders that may result from trauma that also have gender biases are considered as a potential way to understand this difference. Risk and resilience can perhaps more appropriately be considered specific to symptom picture rather than merely development of pathology.


Assuntos
Acontecimentos que Mudam a Vida , Transtornos da Personalidade/psicologia , Transtornos de Estresse Pós-Traumáticos/epidemiologia , Transtornos de Estresse Pós-Traumáticos/etiologia , Violência/psicologia , Adulto , Transtorno da Personalidade Antissocial/psicologia , Transtorno da Personalidade Borderline/psicologia , Cognição , Feminino , Humanos , Masculino , Transtornos da Personalidade/epidemiologia , Prevalência , Estupro/psicologia , Fatores de Risco , Fatores Sexuais , Maus-Tratos Conjugais/psicologia , Transtornos de Estresse Pós-Traumáticos/psicologia , Estresse Psicológico/complicações , Estresse Psicológico/psicologia , Violência/estatística & dados numéricos
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