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Casey, Sherelle. "Cannabinoids for Neuropathic Pain". Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24007.
Pełny tekst źródłaSearle, Robert David. "Acute neuropathic pain following surgery". Thesis, University of Leeds, 2013. http://etheses.whiterose.ac.uk/6321/.
Pełny tekst źródłaChan, A. W. "Neuropathic pain in diabetes mellitus". Thesis, Cardiff University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496046.
Pełny tekst źródłaTurcotte, Dana. "Multiple sclerosis-induced neuropathic pain". The Consultant Pharmacist, 2004. http://hdl.handle.net/1993/23316.
Pełny tekst źródłaLópez, Álvarez Víctor Manuel. "Activity-dependent treatments for neuropathic pain". Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457957.
Pełny tekst źródłaThe onset and maintenance of neuropathic pain following a peripheral nerve injury involves many mechanisms such as changes in transduction, central or peripheral sensitization, and numerous plastic changes at the central level. Usual pharmacological treatments are not sufficient to alleviate the effects of hyperalgesia or allodynia produced by neuropathic pain. Therefore, in this thesis two activity-dependent treatments such as treadmill exercise and electrical stimulation are studied to observe the hypoalgesic effects produced and the molecular mechanisms involved in these beneficial changes. In the first two chapters of this thesis a novel protocol of treadmill exercise is shown, by increasing the velocity progressively during one hour (iTR). It has been shown that other protocols of treadmill ameliorate functional recovery after peripheral nervous system injury but, depending on intensity and duration, different effects have been described. In the first chapter, using an experimental model of neuropathic pain consisting in the section and repair of the sciatic nerve in a rat (SNTR), we found that iTR protocol reduces hyperalgesia by recoding of spontaneous neural activity, reducing neurotrophins levels to counteract nociceptive collateral sprouting, preventing the disruption of chloride cotransporters like NKCC1 and KCC2 to maintain central inhibition and counteracting microglial reactivity at central areas. iTR also positively reduced hyperalgesia in the lateral sciatic area demonstrating that the iTR hypoalgesic effect is not exclusively limited to the blockade of collateral sprouting in the periphery. Changes at central sensory circuits are also important. At the second chapter we found that iTR also increased the activity of serotonergic and noradrenergic projections from brainstem centers partially restoring the central disinhibition induced after the nerve injury. In the third chapter of this thesis, we evaluate the use of peripheral nerve stimulation (PNS) as a passive activity-dependent treatment for neuropathic pain. The therapeutic outcome together with the pattern of peripheral nerve activation, are closely related to the differences in the type and location of electrode, intensity and frequency of stimulation. For this purpose we evaluated two different experimental models as candidates. The spared nerve injury model (SNI) was the initial choice but PNS had very discrete effects in the reduction of mechanical hyperalgesia compared to SNTR. In a preliminary work, we discerned the frequency of stimulation producing the better reduction of hyperalgesia with acute stimulation after injury. Then, we improved the type of electrode and location by designing a system to make chronic stimulation available. We show some results for acute, repetitive acute and chronic stimulation protocols but the best stimulation protocol in reducing mechanical hyperalgesia was iCES protocol. Similarly to iTR, iCES consists of an increasing-frequency pattern of stimulation. We found that iCES triggers a series of changes at central levels, such as the restoration of expression of KCC2 and β2 receptor that act directly on the increase of GABA release in spinal cord facilitating together with the decrease of microglial and astrocytic reactivity, the reduction of mechanical hyperalgesia produced after SNTR.
Wallace, Victoria C. J. "Peripheral nerve demyelination and neuropathic pain". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/27605.
Pełny tekst źródłaTaylor, Anna. "Peripheral mechanisms of trigeminal neuropathic pain". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97105.
Pełny tekst źródłaLa douleur trigeminale neuropathique est une forme unique de douleur qui résulte d'un dommage aux afférents primaires du nerf trijumeau innervant la région de la tête et du coup. Cette douleur constante qui se manifeste en l'absence d'un dommage aux tissus périphériques représente un fardeau social et économique important. Une compréhension rigoureuse des mécanismes qui mènent à cette condition sera nécessaire pour mieux la traiter et préférablement la guérir.La peau de la lèvre inferieure est innervée par des afférents primaires appartenant à différentes classes, incluant les fibres myélinisées Aβ, les fibres légèrement myélinisées Aδ, ainsi que les fibres C non myélinisées. Ensemble, ces fibres peuvent transmettre une variété de stimuli nociceptifs ou inoffensifs tels que rencontrés dans l'environnement. Les stimuli nociceptifs sont majoritairement transmis par les fibres C non myélinisées, lesquelles peuvent être divisées en 2 catégories, peptidergiques ou non peptidergiques, selon des critères neurochimiques et anatomiques. Puisque les lésions nerveuses qui déclenchent la douleur neuropathique se produisent le plus souvent en périphérie, les changements au niveau du système nerveux périphérique sont centraux au développement de la condition douloureuse. Ceci étant dit, l'objectif général de cette thèse est d'explorer les changements périphériques qui se produisent dans un model animal de douleur trigeminale neuropathique.Les résultats de cette thèse sont présentés dans trois chapitres. L'innervation de la peau par les fibres C non peptidergiques chez le rat normal a d'abord été décrite. Ensuite, les changements subis par cette population suivant un dommage au nerf ont été documentés. Suite à un dommage nerveux périphérique, des fibres autonomiques ectopiques ont été observées en proximité des fibres sensorielles en régénération, et ce changement corrélait temporellement avec le phénotype comportemental des animaux. Les niveaux cutanés de GDNF ont rapidement augmenté après le dommage nerveux, fournissant un mécanisme potentiel permettant la régénération des fibres C non peptidergiques et la migration ectopique des fibres parasympathiques. L'ablation des fibres C non peptidergiques a déclenché la pousse des fibres parasympathiques sans changer le comportement des animaux. Par contre, l'ablation de ces fibres chez des animaux neuropathiques a exacerbé la réponse douloureuse de ceux-ci.Ces résultats suggèrent une participation importante des fibres C non peptidergiques et de la migration autonomique dans la douleur neuropathique. De plus, GDNF est rapporté comme étant un facteur pouvant produire ces changements.
Hutton, E. J. "The skin as a window on mechanisms of neuropathy and neuropathic pain". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1532903/.
Pełny tekst źródłaLiu, Xue Jun. "Peripheral regulation of inflammatory pain and neuropathic pain by adenosine". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ66636.pdf.
Pełny tekst źródłaBennett, Michael I. "The development of a pain scale for identifying neuropathic pain". Thesis, University of Birmingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487879.
Pełny tekst źródłaMurai, Nobuhito. "Studies on the analgesic effect of (+)-indeloxazine on neuropathic pain". Kyoto University, 2014. http://hdl.handle.net/2433/193548.
Pełny tekst źródłaFjell, Hjelmström Jenny. "Tetrodotoxin-resistant sodium channels in neuropathic pain /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4181-5/.
Pełny tekst źródłaBennett, Michael I., Nadine Attal, Miroslav M. Backonja, Ralf Baron, Didier Bouhassira, Rainer Freynhagen, Joachim Scholz, Thomas R. Tölle, Hans-Ulrich Wittchen i Troels Staehelin Jensen. "Using screening tools to identify neuropathic pain". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-112626.
Pełny tekst źródłaLowe, Andrew Sheridan. "Functional magnetic resonance imaging of neuropathic pain". Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419854.
Pełny tekst źródłaBennett, Michael I., Nadine Attal, Miroslav M. Backonja, Ralf Baron, Didier Bouhassira, Rainer Freynhagen, Joachim Scholz, Thomas R. Tölle, Hans-Ulrich Wittchen i Troels Staehelin Jensen. "Using screening tools to identify neuropathic pain". Technische Universität Dresden, 2007. https://tud.qucosa.de/id/qucosa%3A26855.
Pełny tekst źródłaNatale, Claudia. "Spinal glycinergic neurotransmission in neuropathic pain models". Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/25376.
Pełny tekst źródłaTam, Denise June. "Role of Glycinergic Neurotransmission in Neuropathic Pain". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16314.
Pełny tekst źródłaTang, Qingbo. "Nonopioid actions of dynorphin and neuropathic pain". Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/289125.
Pełny tekst źródłaGardell, Shannon. "The contribution of descending pain facilitation to the maintenance of neuropathic pain". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289935.
Pełny tekst źródłaSaeed, Abeer Wael. "Chronic neuropathic pain and spinal dorsal horn plasticity". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110356.
Pełny tekst źródłaLa douleur chronique est une condition débilitante ayant de sérieuses répercussions socio-économiques. L'objectif de cette thèse était de mieux comprendre l'organisation de la corne dorsale de la moelle épinière et les changements qui s'y produisent dans les cas de douleurs chronique neuropathique suite à une lésion du système nerveux. Nos études se sont concentrées sur deux composantes importantes des circuits de la douleur: les neurones de projection et leur innervation par les afférents nociceptifs de petit diamètre. Les neurones de projection de la couche 1 de la moelle épinière sont classées selon leur morphologie en 3 types: les neurones fusiformes, multipolaires et pyramidaux. Les deux premiers répondent aux stimuli douloureux et expriment le récepteur de la substance P (NK-1r), alors que les neurones pyramidaux n'expriment ce récepteur qu'occasionellent et répondent au froid non-douloureux. Les deux populations d'afférents principales sont les fibres de petit diamètre peptidergiques, qui expriment la substance P et le "calcitonin gene-related peptide" (CGRP), et les non-peptidergiques, qui sont dépourvues de neuropeptides et qui s'associent avec la lectine IB4. Lors du premier chapitre expérimental, nous avons étudié les changement qui se produisent dans la corne dorsale de la moelle épinière dans un modèle de douleur neuropathique chronique. Nous avons démontré une expression de novo du NK-1r sur les neurones pyramidales, un changement similaire à celui se produisant dans un modèle d'arthrite chronique. Ce changement de phénotype était associé à une augmentation significative du nombre d'appositions peptidergiques faites sur cette population neuronale, qui reçoit habituellement très peu de ces entrées. Afin de vérifier si ces récepteurs sont fonctionnels et répondent aux stimuli douloureux, nous avons injecté de la capsaicine dans la patte arrière, ce qui a mené à une internalisation du récepteur, marquant l'activation de celui-ci. Le deuxième chapitre de cette thèse vérifie si un état de douleur chronique est nécéssaire pour ce changement phénotypique, utilisant une lésion non douloureuse qui cause une augmentation signnificative du NK-1r dans la corne dorsale. Dans ce modèle, une population de nocicepteurs non peptidergiques est excise par une injection dans le nerf sciatique de la toxine saporine conjuguée à la lectine IB4 (IB4-SAP). En absence de symptômes douloureux, la couche 1 de la corne dorsale des animaux lésés a subi une augmentation générale du NK-1r mais sa distribution cellulaire est restée normale, sans expression de novo sur les cellules pyramidales.Lors du troisième chapitre de cette thèse, nous avons vérifié si les neurones de projection de la couche 1 exprimant le NK-1r recevaient des entrées des fibres nociceptives non peptidergiques, comme ce sujet était controversé suite à une publication utilisant des souris transgéniques démontrant une absence de connections de la sorte. Nous avons fait une étude systématique utilisant la microscopie confocale et électronique et avons démontré que les 3 types morphologiques de cellules de projection reçoivent des entrées non peptidergiques directes.Pris ensembles, les résultats de cette thèse suggèrent qu'une condition de douleur chronique est nécessaire pour l'expression du NK-1r sur les neurones pyramidaux et l'augmentation des entrées peptidergiques faites sur celles-ci. D'autres études seront nécessaires pour clarifier l'implication des entrées non peptidergiques faites sur les neurones de projection dans la nociception normale et dans la douleur chronique.
Gkanatsiou, Eleni. "Mass Spectrometry Based Proteomics : Toward understanding neuropathic pain". Thesis, Uppsala universitet, Analytisk kemi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-297658.
Pełny tekst źródłaRockett, Mark Peter. "The contribution of AMPA receptors to neuropathic pain". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29971.
Pełny tekst źródłaO'Neill, Francis. "Mechanistic comparison between spinal and trigeminal neuropathic pain". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29928.
Pełny tekst źródłaHall, Sara M. "Bradykinin Ligands and Receptors Involved in Neuropathic Pain". Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/578606.
Pełny tekst źródłaCAZZATO, Daniele. "Clinical and genetic characterization of neuropathic pain through the model of small fiber neuropathy: implication for diabetic neuropathy". Doctoral thesis, Università degli studi di Ferrara, 2020. http://hdl.handle.net/11392/2478814.
Pełny tekst źródłaNeuropathic pain is a frequent feature in peripheral neuropathy in particular when small nerve fibers, which convey thermal and nociceptive sensations, are involved. Excruciating burning pain at feet and hand is the most common feature of small fiber neuropathy (SFN) which represents a good model for studying neuropathic pain. Voltage gated sodium channel (VGSCs) genes mutations have been found in rare familial painful disorders and more recently, variants in the same genes have been identified in idiopathic and diabetic painful neuropathies, thus widening the spectrum of genetic pain disorders. This PhD thesis aimed at investigating the risk for neuropathic pain in a well-phenotyped cohort of SFN and diabetic neuropathy patients in order to provide a clinical and genetic characterization of patients. The first section focused on the deep-phenotyping of patients with suspected SFN or neuropathic pain through the development of a database for systematic data collection, integration and sharing among clinicians and researchers. Collected data have been used to conduct two retrospective studies. The first study aimed at addressing the diagnostic accuracy of skin biopsy over time comparing the different normative values for intraepidermal nerve fiber density (IENFD) adopted from 1999 to 2019. This study, comparing skin biopsy results in 439 patients according to different cut-off values, showed a significant improvement of skin biopsy diagnostic specificity after the introduction of the age-and-sex-adjusted normative reference values in the 2010, reporting a reduction of false positive of more than 50% when compared with the cut-off values previously adopted. The second study investigated the circadian dynamics of neuropathic pain intensity scored using the numeric rating scale (PI-NRS) in a cohort of 253 patients with suspected painful SFN. This study revealed a circadian pattern of pain features, showing an increase of NRS scores towards the evening, suggesting a possible role for the intra-day PI-NRS variations as adjunctive outcome measure in clinical trials for analgesic drug in SFN-related neuropathic pain. The second section of the thesis provided a genetic characterization of SFN patients. A candidate-gene analysis has been conducted, looking for rare and low frequency genetic variants in VGSCs genes expected to have a large effect on clinical phenotype and describing their frequency in phenotypically well-defined cohorts of SFN patients. The analysis conducted on 1,015 patients grouped according to etiology and painful phenotype showed a slightly higher frequency of VGSCs variants in painful compared to painless phenotype (13.5% and 9.7%, respectively) but no significant differences between diabetes and idiopathic SFN patients (11.5%). Looking at the variants distribution in VGSCs genes, idiopathic and painful patients showed a significant higher frequency of SCN9A variants whereas diabetes and painless patients had more variants in SCN10A gene. However, concerns have been raised about the pathogenicity of single rare gain-of-function variants, since most of them were classified as VUS (variants of unknown significance). Based on these findings, we adopted a new research approach to investigate the risk of neuropathic pain in our diabetic cohort of 513 patients. The work hypothesis relied on a polygenic architecture of painful neuropathy in which all variants, whether rare or common, might contribute with a small effect size to compose the clinical phenotype. Therefore, we computed a polygenic risk score (PRS) combining the weight of each variant identified in a panel of 107 pain-related genes in diabetic neuropathy patients. The PRS was able to discriminate with sufficient accuracy painful from painless patients with an AUC of 60.3%. This study represented the first application of PRS for addressing the risk of neuropathic pain in diabetic neuropathy, pioneering the use of this tool in this clinical context.
Caspani, Ombretta [Verfasser]. "Cold transduction mechanisms during peripheral neuropathic pain / Ombretta Caspani". Berlin : Freie Universität Berlin, 2008. http://d-nb.info/1023169932/34.
Pełny tekst źródłaRose, Kirstin Elizabeth. "The role of the M channel in neuropathic pain". Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521479.
Pełny tekst źródłaChew, Daniel John. "Mechanisms involved in chronic neuropathic pain after avulsion injury". Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/445.
Pełny tekst źródłaBuckley, David A. "Improving the diagnosis and treatment of chronic neuropathic pain". Thesis, University of Huddersfield, 2018. http://eprints.hud.ac.uk/id/eprint/34551/.
Pełny tekst źródłaEmraja, Ahmed M. M. "Animal models of neuropathic pain after spinal cord injury". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4176/.
Pełny tekst źródłaHechler, Ashley C. "Identifying and Treating Neuropathic Pain in Dogs with Syringomyelia". The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1554712901697936.
Pełny tekst źródłaLegg, Ewen. "Behavioural co-morbidities in rat models of neuropathic pain". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9070.
Pełny tekst źródłaMcCormick, Barry. "Antioxidant protection in mitochondria in chemotherapy-induced neuropathic pain". Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=229728.
Pełny tekst źródłaPICCI, CRISTINA. "Exploitation of new pharmacological targets for neuropathic pain reliefe". Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266610.
Pełny tekst źródłaTrovato, A. E. "Endocannabinoid and purinergic systems in rodent neuropathic pain model". Doctoral thesis, Università degli Studi di Milano, 2008. http://hdl.handle.net/2434/63077.
Pełny tekst źródłaSchweinhardt, Petra. "Neural correlates of clinical pain processing in neuropathic and inflammatory pain patients and comparison with experimental pain". Thesis, University of Oxford, 2006. http://ora.ox.ac.uk/objects/uuid:12e71d31-24f8-47e8-ba83-129575007644.
Pełny tekst źródłaYilmaz, Zehra Tijen. "Expression and activity of pain receptors in health and neuropathic pain of the mouth". Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498599.
Pełny tekst źródłaAbdul, Aziz Che Badariah. "Thalamic nociceptiive processing in rat models of acute inflammatory pain and chronic neuropathic pain". Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410465.
Pełny tekst źródłaMyers, Alyssa Michelle. "Single and Combined Effects of Cannabinoids on Neuropathic Pain and Cognition". Master's thesis, Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/378041.
Pełny tekst źródłaM.S.
Rationale. For centuries, medications derived from the marijuana plant have been used for therapeutic purposes across numerous cultures. In 1964, the primary psychoactive ingredient in cannabis, delta-9-tetrahydrocannabinol (-9-THC) was defined. This, followed by the discovery of the endocannabinoid system, marked the beginning of comprehensive research into the beneficial exploitation of this system. The cannabis plant contains various other cannabinoids besides -9-THC. Most of the effects of cannabinoid-based therapies are based on the agonistic action of -9-THC through cannabinoid receptors. Alternatively, some of these effects are caused by the actions of other cannabinoids, like cannabidiol, which does not have high affinity for cannabinoid receptors. Like -9-THC, cannabidiol (CBD), the non-psychoactive phytocannabinoid in Cannabis sativa, has been hypothesized to ameliorate adverse effects of -9-THC. Cannabidiol possesses neuroprotective, antiemetic, and anti-inflammatory properties. Sativex, a 1:1 ratio of CBD and -9-THC, is currently an approved medication in Europe for the treatment of conditions such as neuropathic pain, and has been fast tracked by the USFDA for late stage clinical trials for a host of disorders, ranging from epilepsy to irritable bowel disease. Additionally, increasing preclinical evidence demonstrates that treatment with Cannabidiol alone produces efficacy on a variety of nervous system injuries, including neuropathic pain, schizophrenia and anxiety disorders. Furthermore, there is mounting evidence of an “entourage effect” in cannabinoid-based pharmacotherapies. This effect occurs when treatment with a combination of cannabinoids derived from the plant produce more efficacy than treatment with a single cannabinoid (1). As cannabinoid-based treatments continue to develop and clinical data increases, further investigation of the entourage effect is necessary to facilitate the appropriate future treatment regimens for nervous system disorders. Hypotheses. We hypothesized that treatment with the non-psychoactive cannabis compound cannabidiol would be as effective as the psychoactive cannabis compound -9-THC, or a combination of the two, in mitigating neuropathic pain in a mouse model of chemotherapy-induced peripheral neuropathy. We additionally hypothesized that cannabidiol would not affect classic cannabinoid-agonist induced cognitive impairment in rodent models of learning and memory. Methodology. Neuropathic pain was induced by repeated injections of the chemotherapeutic agent Paclitaxel. Mechanical hypersensitivity to Paclitaxel was assessed using the Von Frey assay. Cognition was assessed using three rodent models of learning and memory: 1) Conditional Discrimination, 2) Conditional Discrimination with a reversal component, and 3) Barnes Maze. Results. Cannabidiol was found to be more potent and more effective than -9-THC in attenuating neuropathic pain in a dose dependent manner. Combinations of CBD+-9-THC revealed that lower, ineffective doses of CBD and -9-THC display supra-additive effects when given in combination while higher, individually effective doses exhibit sub-additive effects in combination. Cognitively, no deficits were observed over a range of doses of any cannabinoid tested in the conditional discrimination tasks, although a slight trend was observed in animals administered the synthetic mixed CB1/CB2 agonist WIN55,212-2. In the Barnes Maze task, treatment with -9-THC alone dose-dependently decreased number of entries and total time spent in the target zone. Cannabidiol did not produce any effects in the Barnes Maze alone, nor did it attenuate the effects seen in animals treated with -9-THC alone. Lastly, -9-THC did not affect total distance traveled or average speed, whereas combination treatment increased both locomotor measurements at all but the highest combination dose. Conclusions. The results of these studies indicate that cannabidiol is more potent than -9-THC in attenuating neuropathic pain. Results of cognitive testing indicate subtle impairment in animals treated with -9-THC and WIN55,212-2 that were not reversed by CBD.
Temple University--Theses
Fiore, Nathan Troy. "Neuroimmune interactions related to development of affective behavioural disturbances in neuropathic pain states". Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20984.
Pełny tekst źródłaKvarnström, Ann. "Neuropathic Pain; Quality of Life, Sensory Assessments and Pharmacological Treatments". Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3766.
Pełny tekst źródłaNeuropathic pain of central and peripheral origin presents a substantial clinical problem as it is often resistant to pharmacological treatment.
The health related quality of life of 126 patients with peripheral neuropathic pain was studied, to provide a cross sectional description from this point of view. Two generic health-related quality of life instruments; the SF-36 and the Nottingham Health Profile were used together with pain assessments, global rating of health and verbal rating scales of pain and other symptoms, as well as patient descriptors.
The analgesic effect of ketamine, lidocaine and morphine were assessed in a double blind, placebo-controlled, randomized study design. Three groups of patients were studied: patients with peripheral neuropathic pain of traumatic origin, patients with central post-stroke pain and patients with neuropathic pain after spinal cord injury. Somatosensory function was examined to see if this could predict response to treatment and to investigate if the drugs caused changes in thermal or mechanical sensibility.
The results shows that the intense pain, limited efficacy and tolerability of available treatments, the low overall rating of health, reduced work status and troublesome symptoms constitute a substantial impact on the quality of life for patients with peripheral neuropathic pain.
The NMDA-antagonist ketamine yielded substantial pain relief to patients with peripheral neuropathic pain and patients with neuropathic pain after spinal cord injury. However, the reported side effects limit the clinical usefulness of the treatment. Lidocaine did not give significant pain relief to the patients in the three studied groups. Morphine may represent a therapeutic alternative for some patients with central post-stroke pain, although only a small group of this category of patients responded with analgesia.
Assessment of baseline somatosensory functions could not be used to identify responders to treatment with either drug, nor did ketamine, lidocaine or morphine cause any changes in thermal or mechanical sensibility.
Ramer, Matthew Stephen. "Sympathetic and sensory neuronal plasticity, peripheral substrates of neuropathic pain". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ31950.pdf.
Pełny tekst źródłaKvarnström, Ann. "Neuropathic pain : quality of life, sensory assessments and pharmacological treatments /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3766.
Pełny tekst źródłaKahlat, Karima. "Role in neuropathic pain of autoimmunity to myelin protein P0". Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544349.
Pełny tekst źródłaMoss, Andrew. "The role of VPAC2 receptors and PKA in neuropathic pain". Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/29898.
Pełny tekst źródłaProudfoot, Clare W. J. "Analgesia mediated by the TRPM8 cold receptor in neuropathic pain". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29953.
Pełny tekst źródłaWong, Shing Chau. "Treatment of neuropathic pain : by Chinese scorpion (Buthus martensii Karsch)". HKBU Institutional Repository, 2011. https://repository.hkbu.edu.hk/etd_ra/1439.
Pełny tekst źródłaErichsen, Helle Kirstein. "Characterisation of the spared nerve injury model of neuropathic pain /". Cph. : The Danish University of Pharmaceutical Scienes, Department of Pharmacology, NeuroSearch, Kongl. Carolinska Medico Chirurgiska Institutet, 2003. http://www.dfh.dk/phd/defences/Hellekirsteinerichsen.htm.
Pełny tekst źródłaBian, Di. "Peripheral and spinal mechanisms of neuropathic pain in the rat". Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284087.
Pełny tekst źródłaBashir, Farhat. "Determining diagnostic indicators for neuropathic pain in patients with osteoarthritis". Thesis, Curtin University, 2021. http://hdl.handle.net/20.500.11937/85465.
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