Acute and subacute diseases causing intrinsic spinal cord damage are confusing and poorly defined clinically and pathologically. of this study is: The purpose 1. To analyse the spectrum of conditions responsible for acute and subacute myelopathy in South Africa. 2. To categorise the clinical presentations and prognosis of the illnesses and to correlate these with aetiology. 3. To assess the validity of diagnostic criteria for acute and subacute myelopathy in general and for the different aetiological groups. 4. To review the literature and to correlate previous studies with the present one. Thirty-four patients fulfilling strict criteria nave been identified over a seven-and-a-half-year period using the Groote Schuur Hospital computer retrieval system. Although the study was essentially retrospective, 11 of these patients were seen personally during their acute illnesses. All these patients have suffered from illnesses causing spinal cord dysfunction in the absence of trauma, physical agents or any extrinsic pressure such as might be caused by tumours or spondylosis. Maximum disability was reached in less than 8 weeks. In 17 patients no cause was identified. The clinical features, laboratory findings and courses have been analysed. Among the results, a high percentage of patients with Brown-Sequard Syndromes were found with possible significance for the pathogenesis of the illness. Seven patients with meningovascular syphilis were analysed as well as 2 additional patients with spinal cord syphilis not fulfilling the strict criteria of the study. Although well known before the penicillin era, this entity is not well described in modern neurological literature. Four patients had myelopathy associated with pulmonary tuberculosis in the absence of tuberculous meningitis or spinal disease. Three of these 4 patients also developed optic neuropathy. The association of these conditions has previously been described in only a very few patients. Two patients had Epstein-Barr virus infections and 1 had an infection with Mycoplasma pneumoniae. Two had systemic lupus erythematosus and 1 had an acute cord infarct following an aortic aneurysm repair. The literature is reviewed and the findings of this study correlated with previous ones. Conclusions regarding terminology, criteria for diagnosis, investigations, course and prognosis are discussed.

Neuromyelitis optica (NMO) is a central nervous system inflammatory demyelinating disorders (CNS IDD) characterized by acute myelitis (AM) and optic neuritis (ON), especially clinically severe longitudinally extensive transverse myelitis (LETM) and simultaneous bilateral ON. Patients with recurrent AM especially LETM without ON, and patients with recurrent ON without AM may have disorders belonging to the spectrum of NMO, neuromyelitis optica spectrum disorders (NMOSD). NMO is likely autoimmune in nature as a significant proportion of patients are seropositive for aquaporin-4 (AQP4) autoantibodies. I studied the clinical features of local Chinese NMOSD patients and their AQP4 autoantibodies seropositivity rates of by indirect immunofluorescence using tissue slides containing primate cerebellum (tissued-based immunofluorescence assay) in patients with 1) NMO, 2) classical multiple sclerosis (CMS), 3) acute disseminated encephalomyelitis (ADEM), 4) single attack or relapsing AM, 5) single attack or relapsing ON, and 6) other neurological disorders. The results showed that NMOSD are severe CNS IDD affecting patients with a wide range of onset ages. Chinese NMOSD patients predominantly have relapsing NMO and relapsing LETM with severe attack of LETM and/or ON. The six-year mortality rate of patients with NMO or relapsing myelitis with LETM was about 12%. Two-thirds of patients have poor neurological outcome at a mean duration of 6.0 years. The results confirmed that AQP4 autoantibodies are specific for NMOSD, and detection of AQP4 autoantibodies is clinically useful for early diagnosis of NMOSD and distinction from CMS. I proceeded to study a cell-based immunofluorescence assay using transfected human embryonic kidney cells overexpressing human AQP4 on cell membrane and found that cell-based assay has higher sensitivity than tissue-based assay in detection of AQP4 autoantibodies in NMO (78% versus 61%). As our NMOSD patients frequently presented clinically with severe brainstem symptoms and signs and lesions in brainstem and other brain regions on magnetic resonance imaging (MRI), I studied the clinical and neuroradiological characteristics of Chinese NMOSD patients with brain involvement. I found that 59% of NMOSD patients have clinical and/or radiological evidence of brain involvement. Importantly, brainstem is the most frequently affected brain region and 24% of NMOSD patients had clinical manifestation of brainstem encephalitis. I also studied the pathogenicity of AQP4 autoantibodies in the absence of complement activation by passive transfer of IgG isolated from sera of NMOSD patients into mice pretreated with complete Freund’s adjuvant (CFA, containing heat-killed mycobacterium tuberculosis) and pertussis toxin (PTx). I observed that pretreatment with CFA and PTx led to breach of BBB in mouse, and IgG isolated from sera of NMOSD patients seropositive for AQP4 autoantibodies led to asymptomatic loss of AQP4 in gray and white matter in mouse spinal cord without inflammatory cell infiltration, demyelination or astrocytic loss in the absence of complement activation (human IgG cannot activate mouse complements). My findings support that 1) AQP4 autoantibodies binding to astrocytic AQP4 per se can cause downregulation of AQP4 in the absence of complement activation, and 2) complement activation with resultant complement activation products play key roles in the inflammation, demyelination and astrocyte cytotoxicity in NMO. / published_or_final_version / Medicine / Doctoral / Doctor of Philosophy

published_or_final_version / Pathology / Master / Master of Medical Sciences

published_or_final_version / Medicine / Master / Master of Medical Sciences

This project was undertaken with the following aims: 1) To generate a data base concerning the management of children with congenital spinal anomalies, who are known to form a significant proportion of the patients being treated in the Department of Paediatric Urology at Red Cross Hospital. 2) To assess the results of the management of these children, with special attention to the goals of therapy, namely preservation of renal function, establishment of urinary continence and protection from urinary tract infection. 3) To compare the treatment methods and results obtained to those reported in the literature. 4) To evaluate critically the treatment methods and results obtained with a view to identifying areas where improvements are possible.

Thesis (MScPhysio (Physiotherapy))--University of Stellenbosch, 2006. / Postoperative rehabilitation programs have shown little efficacy in decreasing pain and disability in short and long term outcomes for lumbar discectomy. Preoperative education in other disciplines of medicine and physiotherapy has shown to decrease pain and disability postoperatively. No studies to date have been published on preoperative education for spinal lumbar surgery patients with radiculopathy. Objective: The objective of this study was to contribute towards further understanding of the preoperative educational requirements of patients undergoing lumbar surgery for lumbar radiculopthy. Method Two surveys were conducted. A new questionnaire was developed for patients to determine their preoperative educational needs regarding spinal surgery due to radiculopathy. These questionnaires were administered at 4-weeks postoperatively to patients from four spinal surgeons in the Greater Kansas City metropolitan area of the US. A second physiotherapist survey was developed and distributed to physiotherapists registered with the Kansas and Missouri State Boards who were actively involved in treating spinal surgery patients in Kansas and Missouri. The data collected from completed questionnaires were analyzed using descriptive and inferential statistical tests....

published_or_final_version / Orthopaedics and Traumatology / Master / Master of Philosophy

Orientador: Marco Antônio Zanini / Banca: Luiz Antonio de Lima Resende / Banca: Rodrigo Bazan / Banca: Silvana Bommarito Monteiro / Banca: Sthela Zanchetta / Resumo: A deficiência de vitamina B12 no ser humano, frequentemente associada a deficiência de fator intrínseco, produzido no estômago, leva a múltiplas alterações neurológicas e hematológicas. A mais conhecida alteração do sistema nervoso central é a desmielinização e degeneração dos fascículos grácil e cuneiforme da medula cervical. Este trabalho teve por objetivo tentar obter um modelo experimental da afecção, através da gastrectomia total em ratos. Animais foram gastrectomizados, submetidos à suplementação polivitamínica via oral, e 2 a 3 meses depois submetidos a estudos de condução nervosa, com estímulos elétricos na extremidade da cauda, e captação de potenciais elétricos em 3 pontos, com distâncias iguais entre si: próximo ao ânus (potencial caudal), região inferior da coluna (potencial lombar) e região da protuberância cervical (potencial cortical). A velocidade de condução pela região inferior da medula espinhal foi denominada segmento V1, pela região torácica alta e cervical até o córtex, segmento V2. Após obtenções de registros de boa qualidade técnica em 15 gastrectomizados, os segmentos V1 e V2 foram comparados com dados de 20 controles pelo teste "t" de Student para amostras independentes, análise de variância (ANOVA) e teste de comparação múltipla de Tukey. Os animais gastrectomizados apresentaram reduções de velocidades estatisticamente significativas para o segmento V2. Os autores pensam ter conseguido modelo experimental da afecção em ratos, o que abre amplas perspectivas para testes terapêuticos em laboratório, com possibilidades para benefícios futuros ao homem / Abstract: The B12 Vitamin deficiency in man, often associated with deficiency of intrinsic factor produced in the stomach, leading to several neurological and hematological disturbances. The best known alteration of the central nervous system is the demyelination and degeneration of the gracilis and cuneiform fascicles in the cervical spinal cord. This study aimed to try an experimental model of the disease, through total gastrectomy in rats. Animals were gastrectomized, submitted to oral polivitaminic supplementation, and 2-3 months later underwent nerve conduction studies. Electrical stimulation was done on the tail end, and electrical potentials were obtained at 3 points with equal distances from each other: near the anus (tail potential), lower spinal cord (lumbar potential) and the region of cervical spinal cord (cortical potential). The conduction velocity of the lower region of the spinal cord segment was named V1, the high spinal cord to the cortex was named V2 segment. After good quality records from 15 gastrectomized animals, the V1 and V2 segments were compared with data from 20 controls by the "t" Student test for independent samples, analysis of variance (ANOVA) and Tukey's multiple comparison test. Gastrectomized animals presented statistically significant reductions in the velocities for the V2 segment. The authors think they have obtained an experimental model of the disease in rats, which opens up broad prospects for therapeutic tests in the laboratory, with possibilities for future benefits to the man / Mestre

Made available in DSpace on 2016-08-12T18:48:50Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-11-11. Added 1 bitstream(s) on 2016-08-12T18:51:08Z : No. of bitstreams: 1 000864494.pdf: 1600996 bytes, checksum: 5adb69b16b5be76806071628d4796075 (MD5) / A deficiência de vitamina B12 no ser humano, frequentemente associada a deficiência de fator intrínseco, produzido no estômago, leva a múltiplas alterações neurológicas e hematológicas. A mais conhecida alteração do sistema nervoso central é a desmielinização e degeneração dos fascículos grácil e cuneiforme da medula cervical. Este trabalho teve por objetivo tentar obter um modelo experimental da afecção, através da gastrectomia total em ratos. Animais foram gastrectomizados, submetidos à suplementação polivitamínica via oral, e 2 a 3 meses depois submetidos a estudos de condução nervosa, com estímulos elétricos na extremidade da cauda, e captação de potenciais elétricos em 3 pontos, com distâncias iguais entre si: próximo ao ânus (potencial caudal), região inferior da coluna (potencial lombar) e região da protuberância cervical (potencial cortical). A velocidade de condução pela região inferior da medula espinhal foi denominada segmento V1, pela região torácica alta e cervical até o córtex, segmento V2. Após obtenções de registros de boa qualidade técnica em 15 gastrectomizados, os segmentos V1 e V2 foram comparados com dados de 20 controles pelo teste t de Student para amostras independentes, análise de variância (ANOVA) e teste de comparação múltipla de Tukey. Os animais gastrectomizados apresentaram reduções de velocidades estatisticamente significativas para o segmento V2. Os autores pensam ter conseguido modelo experimental da afecção em ratos, o que abre amplas perspectivas para testes terapêuticos em laboratório, com possibilidades para benefícios futuros ao homem / The B12 Vitamin deficiency in man, often associated with deficiency of intrinsic factor produced in the stomach, leading to several neurological and hematological disturbances. The best known alteration of the central nervous system is the demyelination and degeneration of the gracilis and cuneiform fascicles in the cervical spinal cord. This study aimed to try an experimental model of the disease, through total gastrectomy in rats. Animals were gastrectomized, submitted to oral polivitaminic supplementation, and 2-3 months later underwent nerve conduction studies. Electrical stimulation was done on the tail end, and electrical potentials were obtained at 3 points with equal distances from each other: near the anus (tail potential), lower spinal cord (lumbar potential) and the region of cervical spinal cord (cortical potential). The conduction velocity of the lower region of the spinal cord segment was named V1, the high spinal cord to the cortex was named V2 segment. After good quality records from 15 gastrectomized animals, the V1 and V2 segments were compared with data from 20 controls by the t Student test for independent samples, analysis of variance (ANOVA) and Tukey's multiple comparison test. Gastrectomized animals presented statistically significant reductions in the velocities for the V2 segment. The authors think they have obtained an experimental model of the disease in rats, which opens up broad prospects for therapeutic tests in the laboratory, with possibilities for future benefits to the man

Law Ka Pui, Karlen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 159-170). / Abstracts in English and Chinese. / Declaration --- p.1 / Abstract --- p.ii / Acknowledgement --- p.vii / Abbreviations --- p.viii / List of Figures --- p.x / List of Tables --- p.xiv / Contents --- p.xvi / Chapter Chapter One - --- Introduction / Chapter 1.1 --- The Cervical Spine / Chapter 1.1.1 --- Anatomy of Typical Cervical Vertebrae --- p.1 / Chapter 1.1.1.1 --- The Vertebral Body / Chapter 1.1.1.2 --- The Vertebral (Neural) Arch / Chapter 1.1.1.3 --- The Vertebral Processes / Chapter 1.1.1.4 --- The Foramina / Chapter 1.1.2 --- Anatomy of Atypical Cervical Vertebrae --- p.6 / Chapter 1.1.3 --- The Cervical Region of Spinal Cord --- p.8 / Chapter 1.1.3.1 --- Structure of the Spinal Cord / Chapter 1.1.3.1.1 --- Gray Matter / Chapter 1.1.3.1.2 --- White Matter / Chapter 1.1.4 --- The Crucial Ascending Tracts in the White Column --- p.11 / Chapter 1.1.4.1 --- Tracts in Dorsal (Posterior) Column / Chapter 1.1.4.2 --- Tracts in the Lateral Column / Chapter 1.1.4.2.1 --- Posterior Spinocerebellar Tract / Chapter 1.1.4.2.2 --- Anterior Spinocerebellar Tract / Chapter 1.1.4.2.3 --- Lateral Spinothalamic Tract / Chapter 1.1.4.2.4 --- Postero-lateral Tract of Lissauer / Chapter 1.1.4.2.5 --- Spino-olivary Tract / Chapter 1.1.4.3 --- Tracts in the Ventral (Anterior) Column / Chapter 1.1.5 --- The Main Descending Tracts of White Column --- p.14 / Chapter 1.1.5.1 --- Tracts in the Dorsal Column / Chapter 1.1.5.2 --- Tracts in the Lateral Column / Chapter 1.1.5.2.1 --- Lateral Corticospinal Tract / Chapter 1.1.5.2.2 --- Rubrospinal Tract / Chapter 1.1.5.3 --- Tracts in Ventral Column / Chapter 1.1.5.3.1 --- Anterior Corticospinal Tract / Chapter 1.1.5.3.2 --- Vestibulospinal Tract and Reticulospinal Tract / Chapter 1.2 --- The Cervical Spinal Nerve Roots / Chapter 1.2.1 --- The Dorsal Roots --- p.16 / Chapter 1.2.2 --- The Ventral Roots --- p.18 / Chapter 1.2.3 --- The Relation between the Afferent and Efferent Nerve Roots --- p.19 / Chapter 1.3 --- Cervical Myelopathy / Chapter 1.3.1 --- Cause of Cervical Spondylotic Myelopathy --- p.21 / Chapter 1.3.2 --- Clinical Symptoms of Cervical Myelopathy --- p.23 / Chapter 1.4 --- Hypothesis --- p.25 / Chapter Chapter Two - --- Methodology / Chapter 2.1 --- Inclusive Criteria of the Study --- p.27 / Chapter 2.2 --- Magnetic Resonance Imaging of the Cervical Spine --- p.29 / Chapter 2.2.1 --- The Setup of the MRI / Chapter 2.2.2 --- Subject Preparation / Chapter 2.2.3 --- Identification of the Most Stenotic Region in the Cervical Spine / Chapter 2.2.4 --- Measurement of the Most Stenotic Cervical Spinal Cord and Canal / Chapter 2.2.4.1 --- Dimensions of the Spinal Cord and Canal in Sagittal Plane / Chapter 2.2.4.2 --- Dimensions of the Spinal Cord and Canal in Coronal Plane / Chapter 2.2.4.3 --- Dimensions of the Spinal Cord and Canal in Horizontal Plane / Chapter 2.2.4.4 --- Compression Ratio of the Sagittal and Coronal Dimension / Chapter 2.2.5 --- Somatosensory Evoked Potential (SEP) Evaluation / Chapter 2.2.6 --- Choice of Stimulation / Chapter 2.2.7 --- Reception of Signals / Chapter 2.2.7.1 --- Erb's Point / Chapter 2.2.7.2 --- Sensory Cortex Reception / Chapter 2.2.7.3 --- Subject Preparation / Chapter 2.3 --- Upper Limb Functional Assessment --- p.44 / Chapter 2.3.1 --- JOA Score for Cervical Myelopathy / Chapter 2.3.1.1 --- Upper Extremity Function / Chapter 2.3.1.2 --- Lower Extremity Function / Chapter 2.3.1.3 --- Sensory Disturbance / Chapter 2.3.1.4 --- Urinary Function / Chapter 2.3.2 --- Jebsen Hand Function Test / Chapter 2.3.2.1 --- Sub-test 2 - Card Turning Test / Chapter 2.3.2.2 --- Sub-test 3 - Small Object Pinching Test / Chapter 2.3.2.3 --- Sub-test 4 - Simulated Feeding Test / Chapter 2.3.2.4 --- Sub-test 5 - Stacking Checkers Test / Chapter 2.3.2.5 --- Sub-test 6 - Large Light Object Picking Test / Chapter 2.3.2.6 --- Sub-test 7 - Heavy Large Object Picking Test / Chapter 2.3.3 --- The Purdue Pegboard Test / Chapter 2.3.3.1 --- Sub-test 1 - Dominant Hand / Chapter 2.3.3.2 --- Sub-test 2 - Non-dominant Hand / Chapter 2.3.3.3 --- Sub-test 3 - Both Hands / Chapter 2.3.3.4 --- Sub-test 4 - Assembly / Chapter 2.4 --- Statistical Analysis Method --- p.74 / Chapter Chapter Three - --- Results / Chapter 3.1 --- Subject Distribution --- p.76 / Chapter 3.2 --- Magnetic Resonance Imaging Measurement --- p.82 / Chapter 3.3 --- Somatosensory Evoked Potentials Recording --- p.94 / Chapter 3.4 --- JOA (Cervical) Scoring --- p.96 / Chapter 3.5 --- Jebsen Hand Function Test Measurement --- p.101 / Chapter 3.6 --- Purdue Pegboard Test Measurement --- p.105 / Chapter 3.7 --- Statistical Analysis Findings --- p.107 / Chapter 3.8 --- Summary --- p.132 / Chapter Chapter Four - --- Discussion / Chapter 4.1 --- Magnetic Resonance Imaging Measurement --- p.134 / Chapter 4.1.1 --- Cervical Myelopathy Subjects has Small Spinal Cord and Canal / Chapter 4.2 --- Somatosensory Evoked Potential of the Median Nerve --- p.140 / Chapter 4.2.1 --- The Latencies were Preserved in Most of the Subjects / Chapter 4.3 --- Cervical Cord Compression Affects the Hand Function Significantly --- p.143 / Chapter 4.3.1 --- Fine Finger Dexterity Deficiency is a Significant Clinical Symptoms of Cervical Myelopathy Subjects / Chapter 4.3.2 --- Deficiency in Manual Dexterity is another Significant Clinical Symptoms of Cervical Myelopathy Subjects / Chapter Chapter Five - --- Summary and Conclusion --- p.153 / Chapter Chapter Six - --- Further Studies / Chapter 6.1 --- Modification in the Sample Recruitment --- p.157 / Chapter 6.2 --- Modification in Assessment Tools and Procedures --- p.158 / Bibliography --- p.159