Patient-reported outcomes in post-traumatic stress disorder. Part II: focus on pharmacological treatment.

Abstract:

:Post-traumatic stress disorder (PTSD) may be associated with long-lasting psychological suffering, distressing psychosocial disability, markedly reduced health-related quality of life, and increased morbidity and mortality in a subgroup of individuals in the aftermath of serious traumatic events. Both etiopathogenesis and treatment modalities of PTSD are best conceptualized within a biopsychosotial model. Pharmacotherapy may lay claim to a major role in the multimodal treatment approaches. Here we outline two different pharmacotherapeutic trends that aim to modify the encoding, consolidation, and rehearsal of traumatic memory in order to reduce the risk of PTSD immediately after trauma exposure on the one hand, and that endeavor to treat the clinical state of PTSD on the other. The theoretical rationales of both pharmacological strategies are the complex neurobiological underpinnings that characterize traumatic memory organization and clinical PTSD. Meanwhile, promising data from randomized controlled trials have been obtained for both approaches. Empirical evidence may inform clinicians in their clinical efforts for this special group of patients. The efficacy of several classes of drugs that have been investigated within a context of research should be evaluated critically and still have to stand the test of effectiveness in daily clinical practice. From a patient perspective, empirical results may serve as a psychoeducative guideline to what pharmacotherapeutic approaches may realistically achieve, what their risks and benefits are, and what their limits are in contributing to reducing the often major chronic suffering caused by serious traumatic events. Ethical issues have to be considered, particularly in the context of pharmacological strategies projected to prevent PTSD in the aftermath of traumatic exposure. :El trastorno por estrés postraumático (TEPT) puede asociarse con un sufrimiento psicológico de larga duración, una perturbadora incapacidad psicosocial, una marcada reducción de la calidad de vida relacionada con la salud y un aumento en la morbilidad y mortalidad en un subgrupo de individuos como consecuencia de acontecimientos traumáticos graves. La etiopatogenia y las modalidades terapéuticas del TEPT son mejor conceptualízadas dentro del modelo biopsicosocial. La farmacoterapía puede demostrar un papel príncipal en las estrategias de tratamíento multimodal. Este artículo resume dos tendencias farmacoterapéuticas diferentes dirigidas a modificar la codificación, consolidación y repetición de la memoria traumática para reducir el riesgo de TEPT inmedíatamente después de la exposición al trauma. Además se revisan los esfuerzos para tratar la sintomatología del TEPT. Los fundamentos teóricos de ambas estrategias farmacológicas son las complejas bases neurobiológicas que caracterizan la organización de la memoria traumática y de los síntomas del TEPT. Por otra parte, se ha obtenido información prometedora en ensayos controlados randomízados para ambas aproximacíones. La evidencia empírica puede informar a los médicos respecto de los esfuerzos clínicos para este grupo especial de pacientes. Se debe evaluar críticamente la eficacia de varias clases de fármacos que se han estudiado en el contexto de la investigación y que todavía tienen que superar la prueba de la eficacía en la práctica clínica diaria. Desde la perspectiva del paciente, los resultados empíricos pueden servir como una orientación psicoeducativa respecto a lo que los enfoques farmacoterapéuticos puedan realmente lograr, a cuáles son sus riesgos y beneficíos, y a cuáles son sus límites en la contribución a la reducción del frecuente y príncipal sufrimiento crónico causado por acontecimientos traumáticos graves. También deben considerarse los aspectos éticos, especialmente en el ámbito de las posibles estrategias farmacológicas para prevenir el TEPT como consecuencia de la exposición traumática. :Chez un sous-groupe de personnes, l'état de stress post-traumatique (ESPT) peut être associé à une souffrance psychologique de longue durée, une incapacité psychosociale éprouvante, une qualité de vie liée á la santé considérablement diminuée et une morbi-mortalité augmentée, dans les suites d'événements traumatiques sévères. Le modèle biopsychosocial est le meilleur moyen de représenter à la fois l'étiopathogenèse et les modalités thérapeutiques de l'ESPT. Le traitement médicamenteux revendique un rôle central dans l'approche multimodale du traitement. Nous présentons ici deux tendances thérapeutiques pharmacologiques différentes qui visent á modifier l'encodage, la consolidation et la répétition de l'événement dans la mémoire traumatique afin, d'une part de diminuer le risque d'ESPT immédiatement après l'exposition au traumatisme, et d'autre part de s'efforcer de traiter l'état clinique de l'ESPT. Les théories de ces deux stratégies s'appuient sur des bases neurobiologiques complexes qui caractérisent l'organisation de la mémoire traumatique et l'ESPT clinique et bénéficient, entre-temps, de données prometteuses issues d'études contrôlées randomisées. Les médecins peuvent être informés par des données empiriques dans leurs efforts pour traiter ce groupe particulier de patients. Les classes médicamenteuses dont l'efficacité a été analysée dans un contexte de recherche doivent être évaluées sérieusement et montrer encore leur efficacité dans la pratique clinique quotidienne. Du point de vue du patient, les résultats empiriques pourraient servir de directive psychoéducative pour ce que les traitements pharmacologiques peuvent réellement réaliser, pour leurs risques et bénéfices et pour leurs limites en termes de diminution de la douleur chronique souvent majeure provoquée par des événements traumatiques graves. Les questions éthiques doivent être prises en compte, particulièrement dans le contexte des strategies médicamenteuses de prévention de l'ESPT dans les suites d'une exposition á un traumatisme.

authors

Kapfhammer HP

subject

Has Abstract

pub_date

2014-06-01 00:00:00

pages

227-37

issue

2

eissn

1294-8322

issn

1958-5969

journal_volume

16

pub_type

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