Naloxone-reversible analgesic response to combat-related stimuli in posttraumatic stress disorder. A pilot study. Arch Gen Psychiat
Manchester Veterans Affairs Medical Center, NH.Archives of General Psychiatry (Impact Factor: 14.48). 07/1990; 47(6):541-4.
We tested the hypothesis that exposure to a stimulus resembling the original traumatic event would induce naloxone-reversible analgesia in patients with posttraumatic stress disorder (PTSD). Eight medication-free Vietnam veterans with PTSD and eight veterans without PTSD, matched for age and combat severity, viewed a 15-minute videotape of dramatized combat under naloxone hydrochloride and placebo conditions in a randomized double-blind crossover design. In the placebo condition, the subjects with PTSD showed a 30% decrease in reported pain intensity ratings of standardized heat stimuli after the combat videotape. No decrease in pain ratings occurred in the subjects with PTSD in the naloxone condition. The subjects without PTSD did not show a decrease in pain ratings in either condition. The results are consistent with the induction of opioid-mediated stress-induced analgesia in the patients with PTSD.
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[Show abstract] [Hide abstract] ABSTRACT: A disturbed beta-endorphin system can be a part of the post-traumatic stress disorder (PTSD) and depression allostasis. Study subjects (N=392) included those with PTSD and/or (stress-induced) depression, and healthy controls with and without traumas. The aim of the study was to examine the network of relations centered around plasma beta-endorphin. The network included anxiety (as a personality trait), traumatic events, pain, aggressiveness, depressive symptoms, and three clusters of PTSD symptoms: intrusions, avoidance, and hyperarousal. Beta-endorphin was represented by individual mean from 13 time points (BEmean), reflecting the total amount of the peripherally secreted hormone, and the coefficient of variation (BEvar), calculated as the ratio of standard deviation to the mean, reflecting the hormone׳s dynamics. BEvar correlated with all other variables, BEmean had no correlations. Structural equation modeling (SEM) was used to examine all interrelations (including their directions) of BEvar and the state/trait variables in the context of their entirety. The model revealed that hyperarousal and anxiety were the only direct agents of peripheral beta-endorphin fluctuations, mediating the effects of other variables. Traumatic events and intrusions act on BEvar via hyperarousal, while depressive symptoms, avoidance, and pain act via anxiety. Hyperarousal should be emphasized as the main agent not only because its effect on BEvar is larger than that of anxiety, but also because it increases anxiety itself (via avoidance and pain). All influences on BEvar are positive and they indicate long-term (sensitizing) effects (as opposed to direct stimulation, for example, by acute pain, anger, etc.). Relations apart from beta-endorphin are also discussed. Copyright © 2015 Elsevier B.V. All rights reserved.
- "The listed phenomena are accompanied by endogenous opioid system dysregulation (Hamner and Hitri, 1992; Lutz and Kieffer, 2013 ). This is confirmed in research with opioid receptor antagonists (Pitman et al., 1990; Glover, 1993). Besides, Risch (1982) and Goodwin et al. (1993) found hightened plasma β-endorphin levels in depression, Kubryak et al. (2012) suggested plasma β-endorphin as an indicator of response to depression treatment, while Darko et al. (1992) obtained correlations of plasma β-endorphin levels with anxiety and phobia in a mixed sample of control and depressed subjects, as well as correlations with obsessions/compulsions in depressed patients only. "
[Show abstract] [Hide abstract] ABSTRACT: Posttraumatic stress disorder (PTSD) and chronic pain frequently co-occur. Patients with comorbid PTSD and chronic pain suffer more distress and disability than patients presenting with only one disorder. The present chapter provides a brief overview of the existing literature on the relationship between PTSD and pain. The goal of the chapter is to provide therapists and researchers with a guide to navigate the literature on this topic by addressing the following questions: (1) Why do PTSD and chronic pain co-occur? (2) Which aspects of this comorbidity should therapists take into account? (3) Are there treatment programs available for patients with comorbid PTSD and chronic pain? (4) What important issues still need to be researched? Finally, some advice regarding clinical practice is provided.
- "Research on SIA in patients with PTSD has produced more consistent 73 findings than research on pain sensitivity and cumulatively suggests that individuals with PTSD report 74 stronger SIA than individuals without PTSD. Pitman et al. (1990) found that exposing veterans to stressful 75 videos (i.e., war-related scenes) provoked an analgesic effect in veterans with PTSD, but not in veterans 76 without PTSD, whose pain tended to increase after watching the video. Mickleborough et al. (2011) found Comprehensive Guide to Post-Traumatic Stress Disorder DOI 10.1007/978-3-319-08613-2_14-1 # Springer International Publishing Switzerland 2015 124 "
- "Abnormal endogenous opioid function has also been found post-trauma. Endogenous opioids are known to facilitate the capacity to gain emotional and psychological distance (Pitman, van der Kolk, Orr, & Greenberg, 1990; van der Kolk, Greenberg, Orr, & Pitman, 1989). In summary, exposure to traumatic events limits the ability of higher-order cortical regions to regulate the intensity and duration of affect. "