Physiological and Biological Testing and Assessment of Post-Traumatic Stress Disorder / Physiological and Biological Testing and Assessment of Post-Traumatic Stress Disorder / Testes fisiológicos e biológicos e avaliação do Transtorno de Estresse Pós-Traumático

This review essay investigates the biological and physi- ological consequences of PTSD to deepen its academic understanding, alongside an analysis of psychobiologi- cal testing and assessment procedures. Psychological responses to traumatic events can be acute stress reactions or stress disorders. One among them is post-traumatic stress disorder (PTSD). When people experience a trau- matic event, such as death, terror, or physical injury, they tend to demonstrate fear, helplessness, or hopelessness. Patients displaying other symptoms like re-experiencing the trauma, avoidance, or hyper-arousal also indicate PTSD. Experiencing extended PTSD may cause significant health problems, whether biological, such as the dysfunction of stress-responsive neurobiological sys- tems, or physiological, such as hypertension and heart disease. Previous studies of trauma survivors reported a strong link between physical and mental health. The cumulative literature in psychology shows that traumatic exposure can cause disturbing effects in the short and long term. This review will contribute to developing an understanding of the biological markers of PTSD. This paper specifically deals with biological and physiological testing and assessment of PTSD. It includes widely utilized biological assessments and summarizes a general multi-model assessment to identify PTSD symptoms.

Las respuestas psicológicas a acontecimientos traumáticos pueden dar lugar a estrés agudo, trastornos de estrés o trastornos de estrés postraumático (TEPT). Cuando las personas experimentan un evento traumático, como la muerte de un ser querido, terror o daño físico, tienden a mostrar miedo, impotencia o desesperanza. Mostrar otros síntomas como volver a vivir aquellas experiencias, evasión o hiperexcitación indica TEPT. Sufrir el TEPT a largo plazo puede causar problemas de salud importantes, ya sean biológicos, como la disfunción de los sistemas neurobiológicos sensibles al estrés; o fisiológicos, como la hipertensión y enfermedades cardíacas. Sin embargo, la literatura psicológica deja poco o ningún espacio para tales consecuencias sobre la salud. Para proporcionar información sobre este tema, la presente revisión tiene como objetivo investigar las consecuencias biológicas y fisiológicas del TEPT, y las pruebas y evaluaciones psicobiológicas relacionadas. Esta revisión de la literatura puede contribuir al desarrollo de marcadores biológicos de TEPT.

As respostas psicológicas a eventos traumáticos po- dem levar a estresse agudo, transtornos de estresse ou transtorno de estresse pós-traumático (TEPT). Quando as pessoas vivenciam um evento traumático, como a morte de um ente querido, terror ou danos físicos, elas tendem a demonstrar medo, desamparo ou desesperança. Mostrar outros sintomas, como reviver essas experiências, evitação ou hiperexcitação, indica TEPT. Sofrer de TEPT de longa duração pode causar problemas de saúde significativos, sejam eles biológicos, como disfunção de sistemas neurobiológicos sensíveis ao estresse; ou fisiológicos, como hipertensão e doenças cardíacas. No entanto, a literatura psicológica deixa pouco ou nenhum espaço para a discussão de tais consequências para a saúde. Para fornecer informações sobre esse tópico, a presente revisão tem como objetivo investigar as consequências biológicas e fisiológicas do TEPT, assim como testes e avaliações psicobiológicas relacionados. Esta revisão de literatura pode contribuir para

The effects of tourniquet on intraocular pressure during knee surgery.

BACKGROUND: In this prospective study we aimed at examining the effects of pneumatic tourniquet on intraocular pressure during elective knee surgery. METHOD: Twenty patients undergoing elective knee surgery under general anesthesia with tracheal intubation were inluded the study. Anesthesia was induced with pentothal, rocuronium and fentanyl, then maintained with sevoflurane and nitrous oxide in oxygen. Intraocular pressure measurements were performed at 7 time points; awake (baseline), following induction, following tracheal intubation, just before tourniquet inflation, after the inflation of tourniquet, before tourniquet deflation, after the deflation of the tourniquet. RESULTS: Baseline IOP was 15 +/- 1 mmHg. Following the induction of anesthesia IOP was reduced significantly (12 +/- 1 mmHg) (p < 0.05), then increased to 16 +/- 1 mmHg after tracheal intubation (p < 0.05). IOP was significantly higher after tourniquet inflation compared with just before (13 +/- 1 mmHg vs 16 +/- 1 mmHg recpectively) (p < 0.05). There was no significant difference between the IOP measurements after the inflation and before the deflation of the tourniquet (p > 0.05). The lowest value was 12 +/- 0 mmHg measured after the tourniquet loosened and it was significant compared with the baseline and the measurement performed before deflation of the tourniquet (16 +/- 0 mmHg) (p < 0.05). CONCLUSION: Pneumatic tourniquet may cause a significant IOP increase in patients performing knee surgery under general anesthesia.

Pretreatment with stellate ganglion blockade before ischemia reduces infarct size in rat hearts.

OBJECTIVE: To investigate the role of stellate ganglion blockade (SGB) in cardio-protection against ischemia reperfusion injury. METHODS: This prospective randomized, experimental study was carried out between August and October 2008 in the Department of Anesthesia, Abant Izzet Baysal University, Bolu, Turkey. Twenty-one rats were randomly divided into 3 groups; group 1--SGB group (rats with percutaneous ganglion blockade), group 2--preconditioned (P) group (rats that were subjected to ischemia and then reperfusion periods for 5 minutes), and group 3--control group (rats that were injected with normal saline). RESULTS: During the ligation period, the length of arrhythmia was significantly shorter in group 2 compared with group 3 (p<0.001). The arrhythmia score in groups 1 and 2 was significantly lower compared with group 3 (p<0.001). In the reperfusion period, the length of arrhythmia was not significantly different in all study groups (p>0.05). But the arrhythmia score was significantly lower both in group 1 and group 3, compared with group 2 (p<0.02). Both in the ischemic and reperfusion periods, the incidence of arrhythmia was lowest in group 1. The infarct size was measured significantly less in groups 1 and 2 compared with group 3 (p<0.001). CONCLUSION: Pretreatment with the left SGB leads to lower arrhythmia scores and reduced infarct size in the Langendorff-perfused rat hearts compared with group 3, but not with group 2.