Browsing by Subject "pain"
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Item Beyond opioid regulation: Why a social and cultural analysis of pain in America is a prerequisite for ethical evidence-based pain policy(2009-05-06) Daniel Goldberg; William J. Winslade; Michele Carter; Melvyn Schreiber; Jason E. Glenn; Howard A. Brody; Ben A. RichThis dissertation constitutes an attempt to understand the social, cultural, legal, and political reasons for the widespread undertreatment of pain in the United States, and to prescribe evidence-based policy recommendations for improving culture and practice as to the treatment of pain. Though the American problems in treating pain have, over the last three decades, produced an abundance of scholarship, practical guides, and policy analyses, relatively little progress has been made. To the contrary, there is evidence that problems in treating pain have worsened, particularly as to disparities in treating pain effectively. It is curious that virtually any handbook of pain management stresses the need for a multimodal approach, but that there exists a paucity of interdisciplinary analyses of pain. Using the lenses of the medical humanities, I complete an interdisciplinary analysis of pain in the United States. Centering on ethics, policy, and the history of medicine, this analysis forms the theoretical framework upon which I erect a series of evidence-based policy recommendations addressing the treatment of pain. The dissertation in itself makes clear to the reader the characteristics of a medical humanities approach to health, illness, and healing.Item Incorporation of analgesics into rodent embryo transfer protocols: assessing the effects on reproductive outcomes(2009-05-15) Burckhardt, Heather AnnSurgical embryo transfer in rodents is a common procedure in today?s research laboratory, although little is known of the effect analgesics may have on not only the recipient female but also the embryos. Two perioperative analgesics, ketoprofen and buprenorphine, were evaluated against a saline control in terms of number of pups born, number of pups weaned, and whether or not a litter was born. Both a uterine approach and an oviduct approach were evaluated. Post-surgical behavior was compared among the three surgical animals in each group, and between the non-surgical analgesic control and its surgical counterpart. Results indicated that ketoprofen and buprenorphine have no effect on the number of pups born, weaned, or litters born when compared to a saline control. Significant differences were found between the non-surgical analgesic control and its surgical counterpart in two behavioral categories; once for ketoprofen (behavior) and once for buprenorphine (physical condition). No other differences were found.Item Reactive oxygen species involvement in gabaergic dysfunction in neuropathic pain(2008-06-18) June Yowtak; Jin Mo Chung, PhD; William D. Willis, MD, PhD; Shawn D. Newlands, MD, PhD; Linda S. Sorkin, PhD; Kyungsoon Chung, PhD; Joel P. Gallagher, PhDNeuropathic pain caused by peripheral nerve damage results in ectopic neuronal excitability, primary sensory neuron degeneration, loss of inhibition by spinal GABAergic neurons and more importantly, the development of central sensitization—increased sensitivity of dorsal horn neurons to stimuli. Oxidative stress due to excessive levels of reactive oxygen species (ROS) has been implicated in the development and maintenance of neuropathic pain. However, it is not known whether oxidative stress is related to the loss of GABAergic tone in the spinal cord. Therefore, the major goal of this work was to elucidate the effects of ROS on GABAergic neuron function and expression.\r\n\r\nThe spinal nerve ligation model (SNL) served as a useful paradigm to study chronic neuropathic pain. SNL mice were produced by tight ligation of the L5 spinal nerve, resulting in increased pain behaviors lasting for many weeks. The paw withdrawal response rates to von Frey filaments measured pain behaviors in the form of mechanical allodynia. Scavenging ROS or increasing spinal GABA neurotransmission produced analgesia in the SNL model. On the other hand, increasing spinal ROS levels or reducing GABA neurotransmission temporarily induced pain behaviors in normal mice. Field recordings demonstrated that the spinal cord dorsal horn neurons were sensitized in SNL mice, and scavenging ROS reduced central sensitization. Blocking GABA neurotransmission significantly reduced this desensitization, indicating that ROS acted mainly upstream to postsynaptic, spinal GABA receptors. Whole cell recordings revealed that elevated levels of ROS increased dorsal horn neuronal excitability but also reduced GABA neuronal excitability. This suggested that ROS may directly contribute to reduced GABA function. Stereological analysis demonstrated that the number of fluorescently tagged GAD67-containing (GABA) neurons is reduced after SNL in the affected spinal dorsal horn. Furthermore, treatment with a ROS scavenger significantly reduced the magnitude of the allodynic behaviors and the SNL-induced loss of GAD67 expression. Therefore, the loss of spinal GABAergic inhibition seen in neuropathic pain may be partly attributed to oxidative stress reducing GABA neuron excitability and promoting the loss of GAD67-producing neurons or down-regulating GAD67 expression. Overall, these studies suggest that ROS play an important role in GABAergic dysfunction that contributes to neuropathic pain.\r\nItem The impact of a noise stressor on capsaicin-induced primary and secondary hyperalgesia(Texas A&M University, 2004-09-30) Grimes, Jeffrey ScottIn searching for new human pain models that more closely resemble clinical pain states, the capsaicin pain model has emerged as a viable model for both inflammatory and neuropathic pain states. A principal benefit of the capsaicin model is that it allows study of two different pain processes, primary and secondary hyperalgesia. Primary hyperalgesia is characterized by spontaneous pain and both heat and mechanical hyperalgesia. In addition, it is likely the result of activation and sensitization of both peripheral and central nociceptors. In contrast, secondary hyperalgesia is characterized by only mechanical hyperalgesia and is caused by the sensitization of central nociceptive neurons. Previous research utilizing the capsaicin pain model has primarily focused on the neural properties with little focus on the impact of affective states on capsaicin-related pain processes. The present study examined the impact of a noise stressor on both primary and secondary hyperalgesia. Results indicated that the effects of the noise stressor impacted secondary hyperalgesia, but not primary hyperalgesia.Item The impact of written emotional disclosure on laboratory induced pain(Texas A&M University, 2005-11-01) Creech, Suzannah K.Previous research has demonstrated the impact of negative emotional states on pain modulation. The direction of this modulation has been shown to correspond to the arousal level and the valence of the emotional state, whether naturally occurring or induced in the laboratory. Other research has consistently linked written emotion disclosure of trauma to better long-term health outcomes among several populations. As most of these studies have focused on long-term health outcome effects of disclosure, little research has been done on the immediate effects of the paradigm on affective or physiological states. This study investigated the short-term effects of written disclosure of trauma on laboratory-induced pain, affective state, and other physiological measures of stress and arousal. Other goals of the study included investigating preexisting differences in pain sensitivity between participants corresponding to lifetime experience of trauma, and determining the degree to which baseline pain testing alters pain sensitivity after emotion induction by creating a conditioned, contextual fear. This is the first study to apply the written emotional disclosure paradigm to laboratory-induced pain.