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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The disturbances observed in animals subjected to unpredictable and uncontrollable aversive events resemble post-traumatic stress disorder (PTSD) symptoms and thus may constitute an animal model of this disorder. It is argued that the similarity between animals' symptoms and those of trauma victims may reflect common etiological factors. Relevant experiments in which animals exhibit generalized fear and arousal, discrete fear of a conditioned stimulus (CS), analgesia, and avoidance are reviewed with the view that these manifestations may be analogous to the PTSD symptom clusters of persistent arousal, reexperiencing, numbing, and avoidance, respectively. Finally, animal paradigms are suggested to test the validity of the model and specific hypotheses are derived from the animal literature regarding trauma variables that are predictive of particular PTSD symptom clusters.
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PMID:Uncontrollability and unpredictability in post-traumatic stress disorder: an animal model. 145 93

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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PMID:Naloxone-reversible analgesic response to combat-related stimuli in posttraumatic stress disorder. A pilot study. 235 Feb 6

The hypothesis that the animal model of inescapable shock (IES) is an appropriate model for posttraumatic stress disorder (PTSD) predicts that re-exposure to a traumatic stressor will precipitate opioid-mediated stress-induced analgesia in people with PTSD. Eight Vietnam veterans with PTSD and eight matched veterans without PTSD viewed a combat videotape under naloxone and placebo conditions in a randomized double-blind crossover design. In the placebo condition, but not after naloxone, the PTSD subjects reported a 30 percent decrease in pain intensity ratings of standardized heat stimuli after the combat videotape. Point biserial correlations revealed that change in pain perception was the most highly correlated with PTSD of all variables tested, including biochemical, physiological, and self-report. These results suggest that a centrally mediated opioid response to traumatic stimuli is an important feature of PTSD. Possible implications of this finding for the psychobiology of PTSD are discussed.
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PMID:Endogenous opioids, stress induced analgesia, and posttraumatic stress disorder. 262 17

Results from studies of pharmacotherapies for primary alcoholism are reviewed, including selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors (e.g. fluoxetine), opiate antagonists (e.g. naltrexone) and dopamine agonists (e.g. bromocriptine). Because there is considerable comorbidity between alcohol dependence, anxiety, and affective disorders, results from studies of medications used to treat these psychiatric disorders are also reviewed, including the 5-HT agonist buspirone and the noradrenergic agent desipramine. The neurobehavioural model of alcohol dependence implies that combinations of medications may lead to more effective treatment; thus, identifying subtypes of alcoholic patients will be important in determining which therapies or combinations of therapy will be most effective in treating alcohol dependence. For example, in an ongoing study, we are attempting to subtype an alcoholic population for treatment selection by measuring endogenous opioid activity. Because endogenous opioids are involved in analgesia, we exposed male and female subjects with alcoholism [some of whom had post-traumatic stress disorder (PTSD)] to cold-induced pain and measured their response before and after administration of naloxone or placebo. The naloxone injection reduced pain response. In addition, women who have PTSD are much more sensitive to stress, which may be related to levels of brain opioid activity.
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PMID:Neurobehavioural basis for the pharmacotherapy of alcoholism: current and future directions. 873

Opioid-mediated analgesia develops in experimental animals following traumatic stress and increased opioid-mediated analgesia has been observed in combat veterans with post-traumatic stress disorder (PTSD). These observations have led to the hypothesis that increased central nervous system (CNS) opioidergic activity exists in patients with PTSD. However, direct CNS data on opioid peptide concentrations and dynamics in patients with PTSD are lacking. We withdrew cerebrospinal fluid (CSF) via a flexible, indwelling subarachnoid catheter over a 6-h period and determined hourly CSF concentrations of immunoreactive beta-endorphin (ir beta END) in 10 well-characterized combat veterans with PTSD and nine matched normal volunteers. Blood was simultaneously withdrawn to obtain plasma for ir beta END. PTSD symptom clusters, as measured by the CAPS, were correlated with neuroendocrine data. Mean CSF ir beta END was significantly greater in patients with PTSD compared with normals and there was a negative correlation between the ir beta END and PTSD intrusive and avoidant symptoms of PTSD. No intergroup difference between plasma ir beta END was found, nor was there a significant correlation between CSF and plasma ir beta END. Immunoreactive beta-lipotropin (ir beta LPH) and pro-opiomelanocortin (irPOMC), both precursors of beta END, were much more plentiful in human CSF than was beta-endorphin itself, as has been previously reported. It remains to be determined whether the increased CNS opioid concentrations predate traumatic stress, thereby conferring a vulnerability to dissociative states and PTSD itself, or result from the trauma. The negative correlation between CSF ir beta END and avoidant and intrusive symptoms suggests that CNS hypersecretion of opioids might constitute an adaptive response to traumatic experience. Poor correlation between CSF and plasma ir beta END limits use of plasma measures to assess CNS opioid activity.
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PMID:Cerebrospinal fluid and plasma beta-endorphin in combat veterans with post-traumatic stress disorder. 937 85

Results from studies of pharmacotherapies for primary alcoholism are reviewed, including selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors (e.g. fluoxetine), opiate antagonists (e.g. naltrexone) and dopamine agonists (e.g. bromocriptine). Because there is considerable co-morbidity between alcohol dependence, anxiety, and affective disorders, results from studies of medications used to treat these psychiatric disorders are also reviewed, including the 5-HT agonist buspirone and the noradrenergic agent desipramine. The neurobehavioural model of alcohol dependence implies that combinations of medications may lead to more effective treatment; thus, identifying subtypes of alcoholic patients will be important in determining which therapies or combinations of therapy will be most effective in treating alcohol dependence. For example, in an ongoing study, we are attempting to subtype an alcoholic population for treatment selection by measuring endogenous opioid activity. Because endogenous opioids are involved in analgesia, we exposed male and female subjects with alcoholism [some of whom had post-traumatic stress disorder (PTSD)] to cold-induced pain and measured their response before and after administration of naloxone or placebo. The naloxone injection reduced pain response. In addition, women who have PTSD are much more sensitive to stress, which may be related to levels of brain opioid activity.
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PMID:Neurobehavioural basis for the pharmacotherapy of alcoholism: current and future directions. 984 37

In this chapter we review trauma-related studies involving epinephrine (E), norepinephrine (NE), and serotonin (5-HT). Central catecholamine neurons seem to play a critical role in level of alertness, vigilance, orienting, selective attention, memory, fear conditioning, and cardiovascular responses to life-threatening stimuli. Evidence of catecholamine dysregulation in post-traumatic stress disorder (PTSD) includes exaggerated increases in heart rate and blood pressure when exposed to visual and auditory reminders of trauma, elevated 24-hour urine catecholamine excretion, decreased platelet alpha-2 adrenergic receptor number, exaggerated behavioral, cardiovascular, and biochemical responses to IY yohimbine, decreased cortical brain metabolism secondary to IV yohimbine, and clinical efficacy of adrenergic blocking agents. Serotonin seems to play numerous roles in the central nervous system, including regulation of sleep, aggression, appetite, cardiovascular and respiratory activity, motor output, anxiety, mood, neuroendocrine secretion, and analgesia. Evidence of serotonergic dysregulation in PTSD includes frequent symptoms of aggression, impulsivity, depression and suicidality, decreased platelet paroxetine binding, blunted prolactin response to fenfluramine, exaggerated reactivity to m-chloro-phenyl-piperazine, and clinical efficacy of serotonin reuptake inhibitors. It has been suggested that alterations in NE, E, and 5-HT may have relevance for symptoms commonly seen in survivors with PTSD, including hypervigilance, exaggerated startle, irritability, impulsivity, aggression, intrusive memories, depressed mood, and suicidality.
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PMID:Neurotransmitter alterations in PTSD: catecholamines and serotonin. 1055 29

Headache is the most common symptom after closed head injury, persisting for more than 2 months in 60% of patients. Rarely does headache occur in isolation. Cervical pain is a frequent accompaniment. Post-traumatic headache is often one of several symptoms of the postconcussive syndrome, and therefore may be accompanied by additional cognitive, behavioral, and somatic problems. Acute post-traumatic headaches may begin at the time of injury and continue for up to 2 months post-injury. Although onset proximate to the time of injury is most common, any new headache type occurring within this period of time is referred to as an acute post-traumatic headache. If such headaches persist beyond the first two months post-injury, they are subsequently referred to as chronic post-traumatic headaches. Over time, post-traumatic headaches may take on a pattern of daily occurrence. If aggressive treatment is initiated early, posttraumatic headache is less likely to become a permanent problem. Once "windup" of post-traumatic headaches occurs, the cycle of ongoing headaches is more difficult to interrupt. The mechanism of post-traumatic headache is poorly understood. Trauma-induced headaches are usually heterogeneous in nature, often including both tension-type pain and intermittent migraine-like attacks. Rebound-headaches may develop from overuse of analgesic medications, and the occurrence of such may complicate significantly the diagnosis of post-traumatic headache. Adequate treatment typically requires both "peripheral" and "central" measures. Understanding the general principles of treatment, especially appropriate use of preventive and abortive medications, will most usefully guide treatment. There is scant literature with which to direct treatment selection for post-traumatic headache. Consequently, treatments for post-traumatic headache are based on those prescribed for phenomenologically similar but etiologically distinct headache disorders. Delayed recovery from post-traumatic headache may be a result of inadequately aggressive or ineffective treatment, overuse of analgesic medications resulting in analgesia rebound phenomena, or comorbid psychiatric disorders (eg, post-traumatic stress disorder, insomnia, substance abuse, depression, or anxiety).
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PMID:Post-traumatic Headache. 1173 6

In a sample of 1550 recently delivered women, traumatic stress after childbirth was studied in relation to obstetric variables. A post-traumatic stress disorder (PTSD) symptom profile and traumatic stress symptoms were assessed by means of the Traumatic Event Scale (TES). Obstetric data comprised delivery mode, duration of the second stage of labor (the time from cervical dilation of 10 cm to partus) and the use of analgesia/anesthesia. Traumatic stress symptoms and having a PTSD symptom profile were both significantly related to the experience of an emergency cesarean section or an instrumental vaginal delivery. It is of clinical importance, however, that most women with a PTSD symptom profile were found in the normal vaginal delivery group (NVD). This implies that a normal vaginal delivery can be experienced as traumatic, just as an emergency cesarian section is not necessarily traumatic. Traumatic stress symptoms were neither substantially correlated to the duration of the second stage of labor, nor to the use of analgesia/anesthesia.
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PMID:Traumatic stress after childbirth: the role of obstetric variables. 1206 Oct 35

The pharmacotherapy of burn care has evolved from the first topical antibiotics instituted > 30 years ago. These have helped greatly to reduce the incidence of burn wound sepsis, but a better understanding of the principles of burn care has resulted in earlier burn wound excision and complete coverage with autograft, cadaver skin, synthetic dressings, and amnion. This has markedly reduced septic complications and ameliorated the hypermetabolic response to burn injury. The hypermetabolic response, which is mediated by hugely increased levels of circulating catecholamines, prostaglandins, glucagon and cortisol, causes profound skeletal muscle catabolism, immune deficiency, peripheral lipolysis, reduced bone mineralisation, reduced linear growth, and increased energy expenditure. Supportive therapy and pharmacological manipulation, acutely and during rehabilitation, with growth hormone, insulin and related proteins, oxandrolone and propranolol can ameliorate the hypermetabolic response, improving survival and long-term outcome. Despite judicious use of topical and systemic antibiotics, opportunistic nosocomial bacterial resistance threatens to annul the improved survival of patients with severe burns. Patterns of emerging resistance encountered in burn units need to be considered, in light of a decreasing antibiotic armamentarium. A holistic approach to pharmacotherapy of severely burned patients including current practice in antimicrobial control, analgesia, sedation, and anxiety management is required. Current therapy of frequently encountered problems, such as post-burn pruritus, prophylaxis of deep venous thrombosis and peptic ulceration, and pharmacological manipulation of inhalation injury in the burned patient is described. Current pharmacotherapy to ameliorate psychosocial problems associated with burns such as acute stress disorder, depression and post traumatic stress disorder are discussed. Better analgesics, newer antibiotics and immune stimulating drugs are required to reduce mortality and morbidity in large burns.
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PMID:Current pharmacotherapy for the treatment of severe burns. 1261 89


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