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Magister Scientiae (Physiotherapy) - MSc(Physio) / The distressing event of Spinal Cord Injury (SCI) leads to complete or incomplete injury, and results in many complications such as such as neurogenic shock, cardiovascular disease, temperature regulatory problems, respiratory complications, dysphagia, thromboembolism, and pressure ulcers amongst others. These complications limit the individual’s functioning and participation. Participation is fruitful and meaningful when you are actively involved in a specific activity. To understand the lack of participation within a specific setting, it is important to know what the limitations in activities are, and what causes these limitations. The goal of rehabilitation should be to reintegrate patients back into the community so that they can fulfil their roles. Aim: The aim of the study was (1) To determine included participants’ socio-demographic and injury characteristics; (2) To describe healthcare services received by people living with long-term Traumatic Spinal Cord Injury (TCSI) over the past 12 months; (3) To determine the point prevalence of common activity limitations of survivors of TSCI four years after injury; (4) To determine the point prevalence of participation restrictions of survivors of TSCI four years after injury; and (5) To determine factors associated with activity limitations and selected participation restrictions four years after injury.

Dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, in fulfilment of the requirements for the degree of Master of Science in Medicine 2015 / Spinal cord injury (SCI) is a devastating injury affecting many South Africans. The purpose of the study was to investigate the relationship between SCI pain and sleep issues during acute inpatient rehabilitation. Seventeen participants were recruited. There were 2 interviews in the study; the 1st interview was done on the day participants were recruited. The 2nd interview was conducted a day before participants were discharged. The time elapsed between the first and second interview was 7.9±2.4. The patients were discharged from the Auckland Rehabilitation hospital (Hope ward). In the 2nd interview the questionnaires for pain, sleep and mood measures were repeated, and two additional questions were asked and the answers recorded for analysis of content. The key findings were; majority of the participants were Black, male (82%). The main cause of traumatic SCI was motor vehicle accident (59%). The common sites of injury were in the legs and neck/shoulder areas in both assessment (admission and discharge). The verbal descriptors that were commonly chosen in both assessments were, “sharp, shooting and tight.” Below level neuropathic pain, followed by musculoskeletal pain were the common types of pain reported. Pain interference was reported greatest in sleep and on average pain intensity was moderate (4-6 on 11-point Numerical Rating Scale). Strong correlations and positive relationships between Pain Catastrophizing Scale and subscales, and with the Pittsburgh Insomnia Rating total scale and subscales were reported in this study. Environmental factors were reported to affect sleep. A high incidence of Restless Leg Syndrome was reported in this study (24%). Depression was commonly reported by participants in both assessments. No significant association was found for the measures of sleep, Restless Leg Syndrome, depression and quality of life and the injury characteristics that were assessed. Significant associations were found at the 95% confidence levels for pain scores and injury characteristics (completeness of injury, level of injury and pain sites). Further studies in this area of pain and sleep management is warranted. It is important that clinicians and researchers in this area find appropriate management for secondary issues which have a severe impact on the daily activities of SCI people, decreasing their quality of life. Key words: SCI pain, sleep disturbances, mood / MT2016

Joie Jie Wang. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 121-132). / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.iii / LIST OF TABLE --- p.vii / LIST OF FIGURES --- p.viii / LIST OF ABBREVIATIONS --- p.xii / Chapter CHAPTER I. --- INTRODUCTION --- p.1 / Chapter I.1. --- Fibre tracts of the rat spinal cord --- p.1 / Chapter I.2. --- Histopathological responses to spinal cord injuries --- p.2 / Chapter I.3. --- Failure of CNS regeneration --- p.4 / Intrinsic inability of CNS neurons themselves to regenerate --- p.4 / Inappropriate synapse without normal functioning --- p.5 / Progressive necrosis and cystic cavities --- p.5 / Autoimmune explanation for the failure of regeneration --- p.6 / Glial scarring --- p.6 / Absence of Schwann cells in the CNS --- p.7 / Lack of requisite growth factors --- p.8 / Chapter I.4. --- The use of transplants --- p.9 / Transplants of fetal nerve tissues --- p.9 / Transplants of peripheral nerve tissues --- p.10 / Transplants of neuroglial cells --- p.11 / Transplants of central neurons --- p.12 / Chapter I.5. --- Objectives of the present study --- p.13 / Chapter CHAPTER II. --- METERIALS AND METHODS --- p.15 / Chapter II.1. --- Hemisection of rats --- p.15 / Chapter II.2. --- Preparation of purified cortical astrocytes --- p.15 / Chapter II.3. --- Scanning electron microscopy (SEM) --- p.18 / Chapter II.4. --- HistologýؤLight microscopy --- p.19 / Chapter II.5. --- Measurement of volume of scar tissue --- p.19 / Chapter II.6. --- Immunofluorescence staining --- p.20 / Chapter II.7. --- Transmission electron microscopy --- p.23 / Chapter II.8. --- Comparison of expression of various proteins in the spinal cord --- p.24 / Polyacrylainide gel electrophoresis --- p.24 / Western blotting --- p.26 / Chapter CHAPTER III. --- RESULTS --- p.28 / Chapter III.1. --- Survival of cultured astrocytes --- p.28 / Chapter III.2. --- Light microscopy --- p.28 / Hemotoxylin and Eosin staining --- p.28 / Toluidine Blue staining --- p.30 / PHAL labelled astrocytes --- p.31 / Immunofluorescence staining --- p.32 / N-CAM --- p.32 / GFAP --- p.33 / NF --- p.34 / Chapter III.3. --- Transmission electron microscopy (TEM) --- p.35 / Chapter III.4. --- Determination of the volume of scar tissue --- p.37 / Chapter III.5. --- Gel electrophoresis --- p.38 / Chapter III.6. --- Immunoblotting and densitometry --- p.38 / Chapter CHAPTER IV. --- DISCUSSION AND CONCLUSIONS --- p.115 / REFERENCES --- p.121

Spinal cord injury (SCI) pathophysiology occurs as a primary traumatic event followed by secondary injury, resulting in the loss of neurons, oligodendrocytes and demyelination of residual axons. Unfortunately, endogenous spontaneous regeneration of oligodendrocytes is minimal. Previously, a method to generate multi-potential stem cells (MPSC) from umbilical cord blood (UCB) has been reported using lineage negative cells (Linneg) grown in fibroblast growth factor 4 (FGF4), stem cell factor (SCF) and fms-like tyrosine kinase receptor-3 ligand (Flt-3l) supplemented serum free medium. These MPSC have the ability to differentiate into bone, muscle and endothelial cells. In this thesis, the ability of MPSC to differentiate into oligodendrocytes was investigated as a potential treatment for SCI. Culturing MPSC under conditions that mimic normal timing of oligodendrocyte differentiation resulted in cells that expressed oligodendrocyte markers in vitro and were morphologically similar to them. I next investigated the ability of MPSC to improve functional recovery in a SCI compression injury model. Although the cells did not differentiate into oligodendrocytes in vivo as we initially hypothesised, a modest but significant improvement in hindlimb function was observed. A cytokine assay revealed that MPSC secrete elevated levels of anti-inflammatory, angiogenic and neurotrophic factors, possibly contributing to indirect mechanisms of repair by reducing secondary injury. Shiverer mouse neonates were next used as an alternative non-injury model to investigate the differentiation potential of MPSC. We hypothesised that transplanting MPSC into a host with an immature immune system and an actively myelinating environment would lead to engraftment and differentiation into oligodendrocytes. However no MPSC that differentiated into oligodendrocytes could be detected. Altogether, our in vitro data adds support for the reprogramming of cells, with further studies needed to test the functionality of resulting oligodendrocyte-like cells. Although MPSC failed to differentiate in both in vivo models, several potential therapeutic targets to treat SCI were found.

Spinal cord injury (SCI) pathophysiology occurs as a primary traumatic event followed by secondary injury, resulting in the loss of neurons, oligodendrocytes and demyelination of residual axons. Unfortunately, endogenous spontaneous regeneration of oligodendrocytes is minimal. Previously, a method to generate multi-potential stem cells (MPSC) from umbilical cord blood (UCB) has been reported using lineage negative cells (Linneg) grown in fibroblast growth factor 4 (FGF4), stem cell factor (SCF) and fms-like tyrosine kinase receptor-3 ligand (Flt-3l) supplemented serum free medium. These MPSC have the ability to differentiate into bone, muscle and endothelial cells. In this thesis, the ability of MPSC to differentiate into oligodendrocytes was investigated as a potential treatment for SCI. Culturing MPSC under conditions that mimic normal timing of oligodendrocyte differentiation resulted in cells that expressed oligodendrocyte markers in vitro and were morphologically similar to them. I next investigated the ability of MPSC to improve functional recovery in a SCI compression injury model. Although the cells did not differentiate into oligodendrocytes in vivo as we initially hypothesised, a modest but significant improvement in hindlimb function was observed. A cytokine assay revealed that MPSC secrete elevated levels of anti-inflammatory, angiogenic and neurotrophic factors, possibly contributing to indirect mechanisms of repair by reducing secondary injury. Shiverer mouse neonates were next used as an alternative non-injury model to investigate the differentiation potential of MPSC. We hypothesised that transplanting MPSC into a host with an immature immune system and an actively myelinating environment would lead to engraftment and differentiation into oligodendrocytes. However no MPSC that differentiated into oligodendrocytes could be detected. Altogether, our in vitro data adds support for the reprogramming of cells, with further studies needed to test the functionality of resulting oligodendrocyte-like cells. Although MPSC failed to differentiate in both in vivo models, several potential therapeutic targets to treat SCI were found.

Thesis (Ph. D.)--University of Missouri-Columbia, 1999. / Typescript. Vita. Includes bibliographical references (leaves 138-148). Also available on the Internet.