Dissertations / Theses on the topic 'Spinal cord'
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Dorsett, Patricia Ann. "Spinal cord injury." Access full text, 2001. http://www.health.qld.gov.au/qscis/PDF/QSCIS_Information/Spinal_Cord_Injury_How_Do_People_Cope.pdf.
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Wrigley, Paul J. "Cold thermal processing in the spinal cord." Connect to full text, 2006. http://hdl.handle.net/2123/1619.
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Thesis (Ph. D.)--University of Sydney, 2007.Title from title screen (viewed May 1, 2007). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Kolling Institute of Medical Research. Includes bibliographical references. Also issued in print.
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Altas, Melanie. "Spinal cord transplants in a rat model of spinal cord injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/MQ49305.pdf.
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Surey, Sarina. "Understanding the molecular mechanisms of spinal cord cavitation after spinal cord injury." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5721/.
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Spinal cord injury (SCI) is a neurodegenerative disease with research centered on axon regeneration and preservation to cure paralysis. Mice and rats are widely studied and experienced models used to imitate SCI due to differences in vascular disruption, blood vessel loss and cavitation at SCI epicenters. This study investigates sub-acute SCI responses, documenting angiogenic/inflammatory factors and matrix deposition in both species. Although cavitation was absent in mice, the lesion site in rats was larger at 8 and 15 days post lesion (dpl). Absence of cavitation in mice correlated with increased levels of pro-angiogenic/wound healing factors within the wound compared to rats at 8 dpl, coinciding with microarray analysis along with increased axonal sparing at T7 and T9 spinal segments. Despite similar deficits in thermal sensitivity 2 hours after injury, by 7 days the responses were comparable to controls in both species. Furthermore, inducing inflammation directly after injury using zymosan resulted in inflammatory-induced angiogenic responses between both species at 8 dpl, contributing to tissue damage and micro-cavities in the CNS. In conclusion angiogenic responses in mice attenuates wound cavitation, reducing secondary axon damage and thus induces axon sprouting/regeneration. These results suggest potential therapeutic utility of manipulating angiogenic/inflammatory responses after human SCI.
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Augutis, Marika. "Pediatric spinal cord injury /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-129-6/.
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Krenz, Natalie. "Plasticity in the rat spinal cord following spinal cord transection, contribution to autonomic dysreflexia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0008/NQ40268.pdf.
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Norrbrink, Budh Cecilia. "Pain following spinal cord injury /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-995-1/.
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Pillay, Robin. "Adult neoplastic spinal cord compression." Master's thesis, University of Cape Town, 2000. http://hdl.handle.net/11427/2888.
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Bibliography : leaves 91-107.Spinal cord compression ( SCC ) constitutes a neurological emergency, and if left untreated, can result in permanent irreversible neurological dysfunction. Disabilities can range from mild weakness to complete quadriplegia with the inherent associated mental, physical and emotional suffering .The burden of cost to the individual and community is enormous.
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Chan, Wing-han Esther. "Road to recovery : adjustment and services needed for those suffering from spinal cord injury /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20131835.
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Weng, Han-Rong. "Functional organization of spinal nociceptive pathways evidence for a modular orgaization of spinal nociceptive reflex systems /." Lund : Dept. of Physiology and Neuroscience, University of Lund, 1996. http://books.google.com/books?id=PclqAAAAMAAJ.
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Wirth, Brigitte Susanne. "Cortico-spinal tract function in incomplete human spinal cord injury." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17602.
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Hunter, Susan M. "Living with traumatic spinal cord injury /." View online ; access limited to URI, 2007. http://0-digitalcommons.uri.edu.helin.uri.edu/dissertations/AAI3276966.
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Boulton, Holly. "Chronic Pain after Spinal Cord Injury." Thesis, University of Southampton, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484857.
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Chronic pain is a common and problematic issue for many individuals with spinal cord injury (SCI; Kennedy, Lude, & Taylor, 2006). Whilst understanding of chronic pain in the general population is increasing, understanding of such pain after SCI remains limited. The literature review explores the issue ofchronic pain after SCI and considers how two dominant models of pain may be applied to chronic pain after SCI. Three pertinent psychological issues are discussed that may play an important role in the maintenance and exacerbation of chronic pain in individuals with SCI; attention, depression, and PTSD. The review stresses that further research into these factors is vital in order to further understanding ofchronic pain in individuals with SCI. The empirical paper focuses of one of the main psychological factors highlighted in the literature review: attentional bias. The study explores whether individuals with SCI and chronic pain possess an attentional bias for pain-related words. Three groups were recruited: chronic pain and SCI (n =14), SCI (n = 15), and healthy controls (n = 15). All participants completed a dot probe computer task that presented pain-related words, pertaining to sensory and affective characteristics ofchronic pain, and neutral words. Words were presented at two exposure durations, 500ms and 1250 ms. Results showed that individuals with chronic pain and SCI possessed an overall attentional bias towards pain related information, in comparison with the other two groups. This difference in attentional bias between the groups was not significantly affected by exposure duration (500ms vs. 1250 ms) or type ofpain words (affective vs. sensory pain words). The general theoretical and clinical implications are discussed, and some suggestions are made for future research
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Mann, Cody Mandeep. "Pharmacological neuroprotection for spinal cord injury." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2758.
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Spinal cord injuries can cause the catastrophic loss of motor and sensory function. The neurological deficits that result are the consequence of not only the primary injury to the spinal cord, but also a complex milieu of secondary pathological processes that are now beginning to be understood. The major mechanisms that underlie this secondary pathology include vascular disruption, ischemia, oxidative stress, excitotoxicity, and inflammation. In light of this, the fact that this secondary pathology occurs after the initial impact makes it potentially amenable to therapeutic intervention. Pharmacotherapies may attenuate some of these processes and minimize secondary damage.
Some of the promising treatments that are emerging for acute spinal cord injury are drugs that are already used by physicians for the treatment of unrelated diseases. These drugs, which have already been established to be safe for humans, offer the unique advantage over other novel therapeutic interventions that have yet to be tested in humans. This would save a tremendous amount of time and money needed for human safety studies, if considered as a treatment for spinal cord injury. Examples of such drugs include minocycline (an antibiotic), erythropoietin (a recombinant hormone used to treat anemia), and statins (a popular class of blood cholesterol reducers), all of which have demonstrated the ability to attenuate the various pathophysiological processes initiated after trauma to the central nervous system.
In a series of studies, erythropoietin, darbepoetin, atorvastatin, simvastatin, and minocycline were all evaluated for their ability to improve neurologic recovery in a clinically relevant model of spinal cord injury. My experiments revealed that erythropoietin, darbepoetin, atorvastatin and minocycline did not significantly improve neurological recovery. These negative results were in stark contrast to the positive findings which had been published in the literature suggesting that differences in experimental models and methodology influence the neuroprotective efficacy of these drugs. Simvastatin, on the other hand, demonstrated significant improvements in locomotor and histological outcomes. Although this is indeed exciting, the results were modest at best. My results highlight the need for further preclinical work on the above treatments to refine and optimize them prior to proposing them for human testing.
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Plemel, Jason Ryan. "Remyelination strategies following spinal cord injury." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42886.
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Peter, Claudio. "Adjustment to spinal cord injury (SCI)." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162256.
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Rakkah, N. I. A. "Electrophysiology of isolated mammalian spinal cord." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233185.
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Al-Zamil, Zeid Muhammed Zeid. "Pharmacology of isolated mammalian spinal cord." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280402.
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Kraemer, Marina. "Novel scaffolds for spinal cord repair." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.591041.
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Injuries to the central nervous system (CNS) have traumatic consequences such as irreparable disability due to the inability of the CNS to regenerate injured nerve fibres. The aim of the work presented here was to develop a scaffold which potentially provides guidance to axons in the injured spinal cord thus facilitating signal transduction. A poly-(lactic-co-glycolic acid) (PLGA, PLA:PGA ratio of 75:25) flat sheet membrane scaffold was created using phase inversion with N-methyl pyrrolidinone (NMP) as the solvent and water as the non-solvent for immersion precipitation. PLGA flat sheet membranes were exposed to surface treatments including aminolysis, peptide immobilisation and ozonation in order to achieve higher cell attachment of PC12 cells, a cell line which was cloned from a solid pheochromocytoma tumour of white rats, and used as a tool for measurement of regeneration. Cell attachment studies revealed no significant difference in cell attachment between modified and not-modified PLGA flat sheet membranes. However, the absence of foetal calf serum (FCS) resulted in fivefold higher cell attachment compared to medium supplemented with 10% FCS. A second scaffold was produced by electrospinning 10% (w/w) PLGA in a chloroform:methanol (CHCl3:MeOH) mixture in ratio of 3:1 resulting in a nanofibrous scaffold. Optimum settings for electrospinning were found to be 3 ml/h feeding rate, 15kV applied voltage and 11cm collector-to-needle distance. Random and aligned PLGA nanofibres were produced, with a fibre diameter of 530±140nm. PC12 cells attached and differentiated to the nanofibrous scaffold. When exposed to NGF these cells stopped dividing and extended neurites. On random fibres, neurite orientation was random, whereas on aligned fibres 63% of neurites grew with the fibre orientation ±15��ᵒ. After 7 days of exposure to NGF, cells had 1-4 neurites on random fibres, reaching a maximum length of 188μm, whereas on aligned fibres, cells had 1-2 neurites, reaching a maximum length of 400μm. PLGA nanofibres were also investigated as a delivery vehicle for bioactive molecules. For this, poly-L-lysine (PLL) was incorporated into electrospun PLGA nanofibres via emulsion electrospinning. PLGA-PLL nanofibres were significantly larger than PLGA nanofibres having a diameter of 830±190nm. In order to visualise the incorporation of PLL, FITC-PLL was electrospun und the resulting nanofibres fluoresced greed. Attachment of PC12s to PLGA-PLL nanofibres was not significantly different compared to PLGA nanofibres. Aligned PLGA-PLL nanofibres were shown to promote neurite outgrowth of PC12s with resulting neurites of up to twice the length compared to aligned PLGA nanofibres. The results suggest that PLGA nanofibres strongly influences neurite organisation, which is potentially useful for future therapeutic approaches. The work in this thesis has shown that electrospun PLGA nanofibre mats have the potential to be used as scaffolds for spinal cord repair addressing topographical guidance and delivery of bioactive molecules to the site of injury.
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Matin, Sajjad S. (Sajjad Shaikh) 1979. "Spinal cord regression via collagen entubulation." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/28889.
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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Aeronautics and Astronautics, 2004.Includes bibliographical references (leaves 51-57).
(cont.) days) post-implantation. Histological and immunohistochemical analyses showed severe fibrous and glial scar formation in Groups I and III, less fibrous scarring in Group II and very little scar manifesting in Groups IV and V. A quantitative analysis of myelinated axons in the center of the explants corresponded with the assessment of scar as a physical barrier to competent axon growth. Groups I and III exhibited the least regenerated axons, Groups IV and V the most. The findings also validated the effectiveness of the dorsal barrier in promoting spinal cord regeneration. Overall, the combination of wrap membrane and dorsal barrier (Group V) proved most effective in creating a hospitable environment for regenerative success.
Traumatic injury to the adult mammalian spinal cord results in varying degrees of lost motor and sensory nerve function. Damaged axons of the central nervous system (CNS) exhibit a severely limited regenerative capacity; paralysis induced by severe trauma is generally permanent. Previous studies have attempted to simulate the peripheral nerve environment, where axonal regeneration is spontaneous, through the implantation of peripheral nerve graft tissue, exogenous growth factors or prosthetic devices. Such intervention has demonstrated the ability of central nerve axons to regrow over significant distances and partially restore distal limb function. The current work aims at evaluating the efficacy of two distinct collagen implants towards promoting spinal cord regeneration. The experimental spinal lesion is a 5mm mid-thoracic gap created by transections at T7 and T9 and removal of intermediary cord and peripheral roots. The two implants offered different entubulation schemes; one implant was a thin walled tube composed of Type I bovine collagen, the other a commercially available bilayered membrane composed of Types I and III porcine collagen. Whereas the tube was fitted directly into the spinal lesion, the membrane was wrapped around the cord stumps like a tubular bandage. Five experimental groups defined the current research: Groups I and II received no implant, Groups III and IV were implanted with tubes, and Group V was implanted with the membrane wrap. A secondary aim of the research was to validate the use of a dorsal barrier in further reducing scar infiltration to the wound. This additional collagen membrane was simply draped over the implant (or lesion) of Groups II, IV and V. Mid-thoracic spinal cord sections were explanted from all groups 4 weeks (28
by Sajjad S. Matin.
S.M.
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Abbaschian, Lara Suzanne 1979. "Spinal cord implants for nerve regeneration." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/28870.
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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Materials Science and Engineering, 2004.Includes bibliographical references (leaves 29-30).
It has only been in the last couple decades that the potential for regeneration in the spinal cord became accepted. However, there is still no proven method for enabling this regeneration. An implant model was developed to help aid in repair, recovery, and regeneration in the spinal cord following spinal cord injury (SCI). This is a polymer-based model with the ability to host neural stem cells. This document briefly reviews the SCI model developed. It also discusses the intellectual property surrounding the implant model, as well as examines the possible pathways through the Food and Drug Administration (FDA) and to the market.
by Lara Suzanne Abbaschian.
M.Eng.
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Tripathi, Richa Balmiki. "Oligodendrogenesis Following Experimental Spinal Cord Injury." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1206114626.
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Divanoglou, Anestis. "The Stockholm - Thessaloniki acute traumatic spinal cord injury study." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-779-5/.
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Ethell, Douglas Wayne. "Analysis of developing chick Gallus domesticus spinal cord proteins using two dimensional gel electrophoresis." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29834.
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Several recent experiments on developing chick spinal cord have established a time window when the developing spinal cord changes from a permissive to a restrictive environment for regeneration. This time window occurs during embryonic days 13-14 (E13-E14) of chick development. Recent experiments in adult rat, have found two proteins that actively inhibit axonal regeneration. This study has sought possible inhibitory proteins, in chicks, correlating to this temporal change. Proteins continuously present after this change (E14-E20) but not before (E11) were identified. Two-dimensional gel electrophoresis was used for separatation of the proteins. Seven protein spots of interest demonstrated this correlative late-expressing neural protein (LNP) profile. Although the functions of these proteins could not be ascertained in this study, further investigation is warranted.Science, Faculty of
Zoology, Department of
Graduate
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Latimer, Amy Ginis Kathleen A. Martin. "Bridging the gap: promoting physical activity among individuals with spinal cord injury within the context of the theory of planned behaviour /." *McMaster only, 2004.
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Reed, Kristin Bodenhamer-Davis Eugenia. "Evaluation of the Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR) in a spinal cord injury population." [Denton, Tex.] : University of North Texas, 2008. http://digital.library.unt.edu/permalink/meta-dc-9045.
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Lim, Siew-Na. "Development of novel therapeutic strategies in spinal cord injury using rodent models of spinal cord compression injury." Thesis, Queen Mary, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538663.
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Li, Ting-hung Darrell. "Ultrastructural imaging of the cervical spinal cord." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B43572285.
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Ryge, Jesper. "Gene expression in rodent spinal neuronal populations and their response to injury." Stockholm : Department of Neuroscience, Karolinska Institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-712-2/.
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Bhatnagar, Timothy. "Quantification of morphological changes of the cervical spinal cord during traumatic spinal cord injury in a rodent model." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52175.
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Traumatic spinal cord injury initiates a complex pathophysiological process that eventually manifests as persistent tissue damage and possible permanent loss of neurologic function. Current experimental models are limited to measuring the gross mechanical response of the spinal cord during injury; thus, little is known about how the internal tissues of the spinal cord deform during injury. The general aims of this research were to develop a method to observe the internal deformations of the in vivo rat spinal cord during clinically-relevant injury models and to determine if the patterns of deformation were correlated to tissue damage manifesting after the injury. To facilitate this work, a novel apparatus and a number of novel methods were developed. First, an apparatus that was capable of inducing contusion and dislocation spinal cord injuries in an in vivo rat model, inside of an MR scanner, was developed. The reported contusion and dislocation injury speeds were comparable with existing spinal cord injury devices, and contusion injury magnitudes showed good accuracy and precision. The device facilitated direct observation and differentiation of the morphological change of the spinal cord tissues during injury. The three-dimensional tissue motion was quantified using a state-of-the-art deformable image registration algorithm that produced displacement fields throughout the volume of the spinal cord around the site of the injury. Furthermore, the image registration methods were validated against a gold-standard. The displacement fields were used to generate transverse-plane mechanical finite strain fields in the spinal cord and the contusion and dislocation injury mechanisms produced distinctly different patterns of tissue deformation in the spinal cord. Lastly, the relationship between mechanical strain and the ensuing tissue damage was investigated in the ventral horns of the gray matter of the spinal cord. This work suggests that compressive strain contributes to the tissue damage in the ventral horns of the gray matter. However, the most important conclusion from this work is that internal observation of the spinal cord tissue during injury provides an invaluable experimental data set that can be used to improve our understanding of the relationship between deformation during injury and manifestation of damage.Applied Science, Faculty of
Mechanical Engineering, Department of
Graduate
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White, Brian Dale Driver Simon. "Identifying changes in resilience during rehabilitation from a spinal cord injury." [Denton, Tex.] : University of North Texas, 2008. http://digital.library.unt.edu/permalink/meta-dc-6039.
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Ghosh, Arko. "A cortical perspective on spinal cord injury /." [S.l.] : [s.n.], 2009. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18202.
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Sliedrecht, Susan. "Counselling Patients with a Spinal Cord Injury." The University of Waikato, 2007. http://hdl.handle.net/10289/2426.
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The aim of this study was to improve current counselling services at the Auckland Spinal Unit. This purpose was achieved by co-researching the topic with people who have extensive experience of living in the community with a spinal cord injury to reveal what they believe was helpful, or believe would have been helpful, in terms of the counselling, when they were newly injured. Listening to the stories of the research participants, through supervision of my own practice, doing a literature review and writing a journal became sources that provided rich knowledges to reflect on my current counselling practice. A qualitative study was conducted using aspects of action research, feminist research and post-structuralist methods. In November 2005, an information pack was mailed to the sixteen patients who had been discharged from the Auckland Spinal Unit between June 2002 and June 2004, who were under the age of sixty -five and lived in the Auckland area, inviting them to participate in this research. Seven people agreed and were available to participate. I interviewed these seven participants, using unstructured interviews. All the interviews were audio-taped and then transcribed verbatim. These verbatim transcripts were then sent back to the participants for any additions/deletions/alterations they chose to make. To initiate the reflecting process, I then went through all the interviews and identified common themes. I understand that if the research participants had been involved in this process, other themes might have emerged for them. The themes identified were loss and grief as a result of a spinal cord injury, sexuality, family (whanau) involvement and how counselling services should be positioned in a setting such as the Auckland Spinal Unit. These themes formed the iii foci of the chapters, with an additional chapter on weaving cultural threads into counselling. The main findings of the study centre on the very important role of counselling at the Auckland Spinal Unit. In particular, the study highlighted the importance of counselling as a place for conversations that make room for multiple positionings and multiple versions of events, a space that respects a patient's hopes, beliefs and dreams for his/her life (which often does not include wheelchairs, catheters and caregivers) but that also supports the patient to make meaning of living life with a spinal cord injury. The study also identified the importance of sexuality counselling. Not including sexuality as a topic in the rehabilitation services provided perpetuates dominant discourses that a person with a spinal cord injury does not want sexual intimacy or cannot be sexually intimate and cannot have children. Family (whanau) involvement in and family's becoming part of the rehabilitation team was very important to most participants. This study looks at how this involvement can be achieved and explores some of the structures currently in place at the Auckland Spinal Unit to facilitate this involvement. Participants in this study expressed a desire for counselling to be highly accessible to both themselves and their families (whanau). They would prefer the counsellors to get to know the patients in their own environment first (in their rooms), so that the patients are positioned to have agency to make choices about how they would like to use the available counselling services. The study concludes with my personal journey of working as a counsellor at the Auckland Spinal Unit and how this research has shaped and fine-tuned my practice.
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Wilsmore, Bradley R. "Thermoregulation in people with spinal cord injury." School of Health Sciences - Faculty of Health and Behavioural Sciences, 2007. http://ro.uow.edu.au/theses/85.
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Thermoafferent information is integrated at multiple levels within the central nervous system. However, due to the difficulty in differentiating thermoregulatory functions of the spinal cord from those of higher centres in humans, the role of the spinal cord in certain aspects of thermoregulation remains unclear. Subjects with spinal cord injury have unique neural changes providing an opportunity to evaluate the role of the spinal cord, independently of higher thermoregulatory centres. Subjects with (N=11) and without (N=11) spinal cord injury were studied in a series of experiments, in which a wide range of local and whole-body temperature changes and postural manipulations were imposed. During these trials, various physiological (skin temperature, core temperature, local sweat rate and sweat expulsion frequency - a measure of central sympathetic drive), and psychophysical variables (thermal sensation and discomfort) were investigated. Six key observations arose from these experiments: (i) Subjects with spinal cord injury had a lower thermoafferent capacity (secondary to neural damage) and a corresponding reduction in thermoefferent drive (sudomotor sensitivity of 4.2 versus 8.8 expulsions•min-1•C-1 in able-bodied; P=0.03). (ii) Equations used to approximate thermoafferent drive in able-bodied subjects, overestimated thermal feedback in subjects with spinal cord injury. However, this could be corrected by modifying the skin area weightings to include only the sensate areas. (iii) No subjects with physiologically-confirmed thermoefferent spinal cord injury displayed sweating from insensate skin sites, indicating that a spinal cord that has been isolated from higher centres cannot induce thermal sweating. (iv) Subjects with spinal cord injury had higher forehead sweat rates (0.77 versus 0.52 mg•cm-2•min-1; P=0.03), but an equivalent sweat sensitivity (1.24 versus 1.27 mg•cm-2•min-1•°C-1; P=0.94), indicating the presence of a peripheral adaptation to sustain thermal homeostasis, and secondary to reduced thermal afferent and efferent flow. (v) Respiratory frequency increased more for a given increase in body temperature in subjects with spinal cord injury (2.4 versus 1.1 breaths•min-1•°C-1; P=0.042), but this did not provide a thermoregulatory benefit. (vi) Subjects with spinal cord injury demonstrated greater changes in behavioural thermoregulatory indicators (thermal sensation and discomfort) in response to standardised local and whole-body thermal loads. Collectively, these observations indicate the unique nature of thermoregulation in people with spinal cord injury and the adaptive ability of the human thermoregulatory system.
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Wicher, Grzegorz. "Clusterin and Megalin in The Spinal Cord." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7365.
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Josephson, Anna. "Spinal cord injury: mechanical and molecular aspects /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-235-3/.
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Widenfalk, Johan. "Trophic factors, neuroprotection and spinal cord repair /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4330-3/.
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Lips, Jeroen. "Experimental spinal cord ischemia detection and protection /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/62717.
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Lee, Jae Ho. "Pharmacological neuroprotection in cervical spinal cord injury." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27239.
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Spinal cord injury (SCI) is a devastating condition that causes paralysis below the level of the injury. To date, there is no convincingly effective treatment. An enormous preclinical and clinical effort is underway to find a treatment, and one approach is to search for pharmacological agents that are already in clinical use (albeit for different indications), but that may also have neuroprotective properties. Examples of such drugs are magnesium, Riluzole (sodium channel blocker), minocycline and statins.
While the majority of human SCI occur in the cervical spinal cord, the vast majority of laboratory SCI research employs animal models of thoracic SCI. An important step, therefore, in the preclinical evaluation of novel treatments is to assess their efficacy in a model of cervical SCI. First, I describe the development of a novel unilateral contusive model of cervical SCI with refined biomechanical, functional, and histological parameters using the Infinite Horizon spinal cord injury device. I conducted a series of experiments in which the spinal cord was injured using various impact forces, impact trajectories, and impact locations off the midline. Behavioral deficits were assessed using a variety of forelimb function tests, after which the cords were evaluated histologically. From these series of experiments, I established a new cervical unilateral spinal cord injury contusion model.
Next, I evaluated the neuroprotective effects of minocycline and simvastatin in the clinically relevant unilateral cervical contusion model. Minocycline is a commonly prescribed tetracycline antibiotic that is prescribed for acne. Simvastatin is one of many hydroxymethylglutaryl-coenzyme-A reductase inhibitors that lower cholesterol. As both drugs have translational potential and have been reported to have neuroprotective properties in various neurological diseases, I assessed the neuroprotective effects of these drugs using a host of functional and histological assessments. In the end, there were no neurological improvements with minocycline or simvastatin treatment after a cervical contusion injury.
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Kramer, John L. K. "Neurological outcomes after cervical spinal cord injury." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/37312.
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In addition to overcoming biological barriers that limit regeneration and repair in the central nervous system after spinal cord injury, clinicians and researchers are faced with the daunting task of assessing the safety and efficacy of therapeutics proposed to ameliorate neurological deficits in humans. While the selection of an appropriate clinical endpoint will depend on a number of factors, including the phase of study and the underlying biological activity, the estimated effect size based on preclinical studies in animal models of spinal cord injury of most therapeutics are expectedly small. A potential promising strategy to detect subtle but clinically meaningful changes in humans is to focus on individual spinal segments partially damaged adjacent to the level of injury.
The primary aim of this thesis was to evaluate the validity of segmental sensorimotor outcomes for the purpose of devising clinical trial endpoints for spinal cord injury. In Chapters Two through Five, I focus this investigation on evaluating sensory outcomes. Chapter Two is chiefly intended to introduce clinical sensory testing methods (i.e. light touch and pinprick) and provide a better understanding of the relationship between the neuropathology of spinal cord injury and afferent anatomy and physiology. In order to address limitations of clinical sensory testing methods, the subsequent three chapters are focused on the application of segmental neurophysiological approaches. More specifically, this involves a series of studies in individuals with spinal cord injury aimed at objectively measuring conduction deficits in the dorsal column and spinothalamic tract based on outcomes from sensory evoked potentials. The thesis then shifts to the segmental assessment of motor function. In Chapter Six, changes in muscle strength are examined in the first year after cervical spinal cord injury, with a specific interest in documenting the relationship between improvements in motor scores in the upper extremities and the recovery of motor levels. This chapter concludes by linking functional independence and neurological outcomes. The discussion that follows is intended to provide an outline of how the knowledge acquired during the course of this doctoral thesis could be translated into phases of a clinical trial program.
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Rathore, Khizr Iqbal. "Iron homeostasis in the injured spinal cord." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86672.
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Iron is essential for life, but its redox activity can render it toxic under certain conditions. Mammalian cells and the organism as a whole have evolved several mechanisms to acquire and utilize iron. The dysregulation of these iron homeostatic mechanisms can cause a number of human diseases and is likely to be a contributing factor in many disorders of the nervous system. Traumatic injuries to the central nervous system (CNS) that result in hemorrhage and cellular disruption can also be associated with impaired iron homeostasis. However, little work has been done to understand the molecular control of iron homeostasis after CNS trauma. The main aim of my thesis research was to investigate the mechanisms underlying the handling of iron after spinal cord injury (SCI) and its impact on secondary pathology and locomotor recovery.In Chapter 2, I carried out a detailed assessment of the localization of iron, and the expression of proteins involved in its trafficking and storage after SCI in mice. This data revealed important and distinct roles for macrophages and astrocytes in iron homeostasis after SCI. In addition, the work showed that iron-loaded macrophages remain at the lesion site for extended periods of time and eventually release their iron, contributing to delayed toxicity. I also examined the role of ceruloplasmin in the iron homeostatic response to SCI using Cp-/- mice. These studies demonstrated that CP plays an important protective role in the injured spinal cord.
In Chapter 3, I sought to further investigate how inflammatory signals (cytokines) may regulate iron homeostasis in astrocytes and microglia. As SCI is known to be associated with a robust inflammatory response involving TNF-a and TGF-b1, I assessed the effects of these cytokines on iron homeostasis in astrocytes and microglia. The studies showed that these two glial cell types exhibit distinct iron homeostatic responses to TNF-a and TGF-b1, and help explain some of the in vivo results seen in SCI. The SCI work also revealed that macrophages phagocytose red blood cells (RBC) at the injury site. I therefore assessed the effects of RBC phagocytosis on the cytokine expression profile of macrophages in vitro. These results (presented in chapter 3) show that RBC phagocytosis results in a switch from pro-inflammatory to anti-inflammatory cytokine expression; thus suggesting that macrophages that have phagocytosed RBCs in SCI may be anti-inflammatory and pro-fibrogenic in nature. Finally in Chapter 4, I examined the role of the iron binding protein Lipocalin 2 (Lcn2) in SCI. In this chapter I show that the expression of Lcn2 and its receptor are increased in CNS cells, as well as certain types of invading immune cells after SCI. Using Lcn2-/- mice, I show that Lcn2 plays a detrimental role, and that it contributes to inflammation and secondary cell death after SCI.
Together the results presented in this thesis shed light on the iron homeostatic response and its interplay with inflammation in spinal cord injury.
Le fer est essentiel pour les organismes vivants. Toutefois, son pouvoir oxydoréducteur peut le rendre toxique dans certaines conditions. Les mammifères ont développé plusieurs mécanismes cellulaires pour capter et utiliser le fer, or le dérèglement de ces derniers peut mener à de nombreuses maladies chez l'homme. Plus spécifiquement, des défauts de l'homéostasie ferrique sont impliqués dans de nombreuses pathologies du système nerveux central (SNC), comme par exemple les lésions traumatiques menant à des hémorragies et des lyses cellulaires. Néanmoins, très peu d'études ont été entreprises à ce jour pour comprendre les mécanismes moléculaires contrôlant l'homéostasie du fer qui se mettent en place à la suite de traumatismes du système nerveux. Le but principal de ma thèse a été d'étudier les mécanismes moléculaires de prise en charge du fer après des lésions de la moelle épinière (LME), ainsi que leurs impacts sur les pathologies secondaires liées à ces lésions et le rétablissement de la locomotion.
Une évaluation détaillée de la localisation du fer et des protéines impliquées dans son transport et son stockage après induction de LME chez la souris a été entreprise (chapitre 2). Ces analyses ont révélé que les astrocytes et les macrophages jouent un rôle primordial et distinct dans l'homéostasie ferrique. En effet, cette étude a démontré que pour contribuer à retarder la toxicité, les macrophages chargés de fer demeurent sur le lieu de la lésion durant une période prolongée avant d'éventuellement relâcher leur fer. J'ai également examiné le rôle de la ceruloplasmine en utilisant des souris Cp-/-, révélant que cette dernière protège la moelle épinière lors de lésions.
Ensuite, j'ai poursuivi mes investigations pour savoir comment les signaux inflammatoires tels que les cytokines peuvent réguler l'homéostasie ferrique des astrocytes et des microglies (chapitre 3). Les LME sont connues pour être associées à une forte réponse inflammatoire qui implique les cytonkines TNF-a et TGFb1. En conséquence, j'ai évalué les effets de ces dernières sur l'homéostasie ferrique des astrocytes et des microglies. Ces études ont démontré que ces deux types de cellules gliales possèdent une homéostasie ferrique distincte en réponse au TNF-a et TGFb1, pouvant expliquer certains effets des LME observés in vivo. Les études sur les LME ont révélé que les macrophages peuvent phagocyter les globules rouges (GR) au niveau du site de la lésion. J'ai donc entrepris d'étudier les effets de la phagocytose des GR sur le profil d'expression des macrophages in vitro. Les résultats obtenus montrent que la phagocytose des GR induit un transfert d'expression de cytokines pro-inflammatoires à anti-inflammatoires. Cette observation suggère que les macrophages ayant phagocytés les GR lors de LME pourraient êtres de nature anti-inflammatoire et pro-fibrogène.
Finalement, j'ai examiné le rôle de la protéine Lipocaline2 (Lcn2) lors de LME (chapitre 4). Les Lcn2 sont des protéines complexant le fer. J'ai démontré que leur expression ainsi que celle de leurs récepteurs était augmentée dans le SNC suite à des LME, tout comme certains types de cellules envahissantes du système immunitaire. L'utilisation de souris Lcn2-/- m'a permis de démontrer que Lcn2 joue un rôle nuisible en contribuant à la mort cellulaire post- LME par des voies inflammatoires et secondaires. Les résultats présentés dans cette thèse ouvrent de nouvelles connaissances sur l'homéostasie ferrique et la réponse inflammatoire réciproque lors de lésions de la moelle épinière.
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Rolfe, Madeleine. "Childbirth for women with spinal cord injuries." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510429.
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Li, Ting-hung Darrell, and 李廷雄. "Ultrastructural imaging of the cervical spinal cord." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B43572285.
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Tegg, Sophie Louise. "Psychological adjustment to traumatic spinal cord injury." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327331.
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Wang, Difei. "Chondroitinase ABC in chronic spinal cord injury." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609828.
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Dickie, Allen Charles. "Spinal cord plasticity in peripheral inflammatory pain." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9547.
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Inflammatory pain is a debilitating condition that can occur following tissue injury or inflammation and results in touch evoked pain (allodynia), exaggerated pain (hyperalgesia) and spontaneous pain, yet the neural plasticity underlying these symptoms is not fully understood. However, it is known that lamina I neurokinin 1 receptor expressing (NK1R+) spinal cord output neurons are crucial for the manifestation of inflammatory pain. There is also evidence that the afferent input to and the postsynaptic response of these neurons may be altered in inflammatory pain, which could be relevant for inflammatory pain hypersensitivity. Therefore, the aim of this thesis was to study inflammatory pain spinal plasticity mechanisms by investigating the synaptic input to lamina I NK1R+ neurons. In ex vivo spinal cord and dorsal root preparations from the rat, electrophysiological techniques were used to assess inflammation-induced changes in and pharmacological manipulation of the primary afferent drive to lamina I NK1R+ neurons. The excitatory input to lamina I NK1R+ neurons was examined and it was found that inflammation did not alter the relative distribution of the type of primary afferent input received and did not potentiate monosynaptic A δ or monosynaptic C-fibre input, the predominant input to these neurons. Spontaneous excitatory input was significantly elevated in the subset of neurons that received monosynaptic A δ-fibre input only, regardless of inflammation. It has recently been shown that the chemerin receptor 23 (ChemR23) represents a novel inflammatory pain target, whereby ChemR23 agonists can decrease inflammatory pain hypersensitivity, by a mechanism that involves the attenuation of potentiated spinal cord responses. This study has found that the ChemR23 agonist, chemerin, attenuated capsaicin potentiation of excitatory input to lamina I NK1R+ neurons and significantly reduced monosynaptic C-fibre input to a subset of these neurons in inflammatory pain. However, chemerin was without effect in non-potentiated conditions. In exploring potential inflammatory pain spinal plasticity mechanisms, I have investigated a phenomenon called activity-dependent slowing (ADS), whereby repetitive stimulation of C-fibres at frequencies of 1Hz or above results in a progressive slowing of action potential conduction velocity, which manifests as a progressive increase in response latency. This is proposed to limit nociceptive input to the spinal cord, thus regulating plasticity. Results demonstrate that inflammation significantly attenuated C-fibre ADS in isolated dorsal roots. Furthermore, ADS in monosynaptic C-fibre input to lamina I NK1R+ neurons was significantly reduced in inflammatory pain, which could facilitate nociceptive drive to these key spinal cord output neurons and promote inflammatory pain spinal cord plasticity. In conclusion, the major novel findings of this thesis are firstly, that chemerin can attenuate primary afferent input to lamina I NK1R+ neurons in potentiated conditions, which supports recent studies that suggest ChemR23 is a potential target for the development of new analgesics. Secondly, it was discovered that ADS in monosynaptic C-fibre inputs to lamina I NK1R+ neurons is altered in inflammatory pain, which could be relevant for inflammatory pain spinal plasticity. The findings presented in this thesis could contribute to the development of novel inflammatory pain treatments.
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Doyle, Christopher Alfred. "Catecholaminergic innervation of the cat spinal cord." Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/29736.
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The organisation of catecholamine (CA)-containing nerve terminals in the cat spinal dorsal horn was examined in an immunocytochemical study employing antisera against tyrosine hydroxylase & dopamine-β-hydroxylase. Light microscopic analysis revealed that varicose axons were concentrated in laminae I, II & IV. Correlated ultrastructural analysis showed that these terminals usually formed single synapses with dendrites of somata, but not with other axon terminals. This suggests that descending catecholaminergic axons regulate sensory transmission through the dorsal horn via a postsynaptic action upon dorsal horn neurons. Using the retrograde tracer horseradish peroxidase to label particular groups of dorsal horn neurons, it was shown that the postsynaptic dorsal column (PSDC) pathway, is a major protection target of CA-containing axons. Over 60% of these cells were found to have dopamine-β-hydroxylase immunostained varicosities closely apposed to their somata and/or proximal dendrites, and correlated ultrastructural analysis confirmed that many of these contacts were regions of synaptic association. In contrast, the cells of the spinocervical tract (SCT) did not receive a major innervation from these axons. The lateral cervical nucleus (LCN), the termination site of SCT cells, was found to possess a dense innervation from CA-containing axons. These fibres were present throughout the nucleus and synapsed with dendrites and somata, including those of large cells in the lateral region, but not with other axon terminals. This suggests that catecholaminergic axons in the LCN regulate the activity of LCN neurons but not the terminals of SCT cells. It has been suggested that many catecholaminergic axons in the dorsal horn may contain neuropeptide Y (NPY), and an examination was made of NPY-immunoreactive axons to test this hypothesis. Light microscopy revealed a heavy concentration of NPY-positive profiles in laminae I & II, but only low to moderate numbers in III-VI.
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Moffitt, Michael Adam. "Functional Imaging of the Mammalian Spinal Cord." Case Western Reserve University School of Graduate Studies / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=case1081363883.
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Hillyer, Jessica Erin. "Enhancing Locomotor Recovery after Spinal Cord Injury." Kent State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=kent1216910376.
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Mohrman, Ashley E. "Regenerative Medicine Approaches to Spinal Cord Injury." University of Akron / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=akron1491495476427594.
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