Relevant bibliographies by topics / Spinal cord disease

Academic literature on the topic 'Spinal cord disease'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Spinal cord disease"

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Schiff, David. "METASTATIC SPINAL CORD DISEASE." CONTINUUM: Lifelong Learning in Neurology 11 (October 2005): 30–46. http://dx.doi.org/10.1212/01.con.0000293678.78683.34.

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Morita, Masahiro, Akira Miyauchi, Shinya Okuda, Takenori Oda, Tomio Yamamoto, and Motoki Iwasaki. "Charcot spinal disease after spinal cord injury." Journal of Neurosurgery: Spine 9, no. 5 (November 2008): 419–26. http://dx.doi.org/10.3171/spi.2008.9.11.419.

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Object The authors investigated the background, risk factors, and treatment strategies for Charcot spinal disease (CSD) after spinal cord injury (SCI). Methods The authors retrospectively examined the clinical and radiological findings in 9 patients with a total of 10 Charcot spine lesions that occurred after SCI. The mean age of the 9 patients was 54 years, and all patients presented with complete SCIs. In all but 1 patient, symptoms did not develop until 10 years postinjury. All 10 Charcot spine lesions were located below the thoracolumbar junction. Surgical treatment was performed in 7 patients (7 lesions), and the mean duration of postoperative follow-up was 84 months. Results All patients reported audible noises when changing posture, 5 of 9 patients reported low-back pain, and 7 patients displayed increasing instability while sitting. In 8 patients, spasticity disappeared and limbs became flaccid several years after SCI. Two patients had associated bacterial infections in the Charcot spine lesions, and 1 patient complained of autonomic dysreflexic symptoms associated with trunk movements. Although postoperative complications occurred in 3 patients, all patients who underwent surgical treatment made a good recovery and were able to return to daily life in a wheelchair. On lateral radiography, the mean range of motion at the lesion site was 43°, and fluid collections between the involved vertebrae were observed in 8 patients on MR images; ankylosing spinal hyperostosis was observed in 7 patients. Charcot spine lesions tended to occur at the junction between or at the end of an ankylosing spinal hyperostotic lesion. Postoperatively, solid arthrodesis was obtained within 6 months in all surgically treated lesions. Conclusions Disappearance of spasticity in the lower extremities is thought to be an important physical sign suggestive of CSD after SCI. Sitting imbalance and the fluid volume of the Charcot spinal lesions are related to range of motion at the lesion site. In addition to a combined approach, a single posterior approach with acquisition of anterior support is an option for surgical treatment even in cases of infected CSD.
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Lee, Hyung Seok, Do Young Kim, Ha Young Shin, Young-Chul Choi, and Seung Min Kim. "Spinal cord involvement in Behçet’s disease." Multiple Sclerosis Journal 22, no. 7 (October 19, 2015): 960–63. http://dx.doi.org/10.1177/1352458515613642.

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Background: Spinal cord involvement in Behçet’s disease is not well studied. Objective: To evaluate the clinical, laboratory and magnetic resonance imaging characteristics of spinal cord involvement in Behçet’s disease. Methods: We retrospectively reviewed 10 spinal cord involvements in seven patients with Behçet’s disease. Results: The median age of onset for spinal cord involvement was 32 (23–45 years). Two patients showed a secondary progressive course. Cerebrospinal fluid findings revealed mild to moderate pleocytosis and/or elevated protein levels. In eight spinal cord involvements, the lesion was longer than three vertebrae. Serum anti-aquaporin-4 antibody was negative in all four patients tested. Conclusions: Longitudinally extensive transverse myelitis is a characteristic manifestation of spinal cord involvement in Behçet’s disease.
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Goldblatt, Jack, Peter Keet, and Desmond Dall. "Spinal Cord Decompression for Gaucher's Disease." Neurosurgery 21, no. 2 (August 1, 1987): 227–30. http://dx.doi.org/10.1227/00006123-198708000-00017.

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Abstract We report an individual with Type I nonneuronopathic Gaucher's disease who experienced the rare complication of spinal cord compression secondary to a sclerotic vertebral fracture. He successfully underwent anterolateral spinal cord decompression and spinal fusion despite the severity of his generalized skeletal disease.
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Agrawal, Dr Umang, and Dr Sujata Tripathi. "Metastatic Adenocarcinoma lung Mimicking Spinal Tuberculosis (Pott's disease) in a female Presenting with Spinal Cord Compression." International Journal of Scientific Research 2, no. 7 (June 1, 2012): 338–39. http://dx.doi.org/10.15373/22778179/july2013/115.

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R.T, Ross. "Spinal Cord Infarction in Disease and Surgery of the Aorta." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 12, no. 4 (November 1985): 289–95. http://dx.doi.org/10.1017/s0317167100035368.

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ABSTRACT:Diseases of the aorta and surgery of the aorta can produce spinal cord damage. There are major variations in blood supply to the spinal cord between individuals. The spinal cord may be tamponaded by increased spinal fluid pressure subsequent to clamping the aorta. Both of these factors may contribute to spinal cord infarction. The available methods and procedures to protect the spinal cord during surgery are discussed.
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YANAGI, TSUTOMU. "MRI diagnosis of spinal cord disease." Nihon Naika Gakkai Zasshi 84, no. 9 (1995): 1588–93. http://dx.doi.org/10.2169/naika.84.1588.

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Gupta, Vineeta, Arvind Srivastava, and Baldev Bhatia. "Hodgkin Disease With Spinal Cord Compression." Journal of Pediatric Hematology/Oncology 31, no. 10 (October 2009): 771–73. http://dx.doi.org/10.1097/mph.0b013e31819c1ff0.

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Myers, Jonathan, Matthew Lee, and Jenny Kiratli. "Cardiovascular Disease in Spinal Cord Injury." American Journal of Physical Medicine & Rehabilitation 86, no. 2 (February 2007): 142–52. http://dx.doi.org/10.1097/phm.0b013e31802f0247.

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Schmitt, James, Meena Midha, and Norma McKenzie. "Medical Complications of Spinal Cord Disease." Neurologic Clinics 9, no. 3 (August 1991): 779–95. http://dx.doi.org/10.1016/s0733-8619(18)30279-2.

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Dissertations / Theses on the topic "Spinal cord disease"

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Wahman, Kerstin. "Cardiovascular disease prevention after spinal cord injury : a new challenge /." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-936-2/.

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Nelvagal, Hemanth Ramesh. "Spinal cord pathology in CLN1 disease : a novel therapeutic target." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/spinal-cord-pathology-in-cln1-disease(8b1dc3ed-dfd9-442d-a427-43ded0d82a6a).html.

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The neuronal ceroid lipofuscinoses (NCLs) are a group of up to 14 inherited progressive neurodegenerative lysosomal storage disorders affecting children and young adults. Together, they are the most common pediatric neurodegenerative storage disorders. Symptoms include loss of vision, epileptic seizures and the loss of cognitive and motor function. A lack of any effective therapies means that all forms are fatal. CLN1 disease or Infantile NCL is one of the most rapidly progressing forms of the disease and is caused by a deficiency of the lysosomal enzyme palmitoyl protein thioesterase – 1 (PPT1). Ppt1 deficient (Ppt1-/-) mice recapitulate features of the human disease and have proved to be a useful tool in characterizing disease progression and pathology in the brain. However, these pathological changes fail to fully explain the sensorimotor deficits seen in this mouse model as well as in human CLN1 disease. Along with the limited success of various brain directed therapies, this led us to analyze the spinal cord. Our analysis revealed unexpectedly profound and rapidly progressing disease pathology in the spinal cords of these mice, which occurs earlier than similar events in the brain. This included regional atrophy, neuroinflammation, and significant neuron loss at all levels of the cord as well as novel phenotypes indicating a postnatal developmental delay and significant white matter pathology. Automated gait analysis also showed novel early phenotypes in these mice including an increased dependence on the forelimbs for locomotion. Similar spinal cord pathology was also demonstrated in human INCL autopsy samples as well as in mouse models of the other major forms of NCL. Targeting the spinal cords of Ppt1-/-mice with enzyme replacement therapy (ERT) and gene therapy significantly improved disease pathology, motor function and lifespan in these mice, demonstrating the clinical significance of spinal cord pathology in these mice. Furthermore, combining intracranial and intrathecal gene therapy showed a synergistic effect, showing the greatest improvements for any CLN1 disease therapy to date. Taken together, these findings highlight the spinal cord as not only being significantly affected in CLN1 disease, but also as a novel and effective therapeutic target.
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Rogers, A. T. "Spinal cord cell culture : a model for neuronal development and disease." Thesis, University of Bath, 1988. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234048.

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Flank, Peter. "Spinal cord injuries in Sweden : studies on clinical follow-ups." Doctoral thesis, Umeå universitet, Rehabiliteringsmedicin, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-125202.

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A spinal cord injury is a serious medical condition, often caused by a physical trauma. An injury to the spinal cord affects the neurotransmission between the brain and spinal cord segments below the level of injury. The SCI causes a loss of motor function, sensory function and autonomic regulation of the body, temporary or permanent. Significantly improved acute care, primary comprehensive rehabilitation and life-long structured follow-up has led to persons with spinal cord injury (SCI) living longer than ever before. However, increased long-time survival has allowed secondary conditions to emerge, like diabetes mellitus and where cardiovascular disease (CVD) now is the most common cause of death among SCI patients. Other possible CVD-related comorbidities in this patient group have been reported to be pain and mood disturbances. There is still lack of, and need for more knowledge in the field of CVD-related screening and prevention after SCI. The overall aim of this thesis was to contribute to a scientific ground regarding the need for CVD-related screening and prevention after SCI. In Paper I and Paper II, patients with wheelchair-dependent post-traumatic SCI (paraplegia) were assessed. The results in paper I showed that 80% of the examined patients had at least one cardiovascular disease risk marker irrespective of body mass index (BMI). Dyslipidemia was common for both men and women at all BMI categories. The study also showed a high prevalence of hypertension, especially in men. Paper II showed a low frequency of self-reported physical activity, where only one out of 5 persons reported undertaking physical activity >30 min/day. The physically active had lower diastolic blood pressure but no significant difference in blood lipids. In paper III and IV, patients with SCI (tetraplegia and paraplegia) participated in the studies. Eighty-one percent of the patients had dyslipidemia, where also a majority of the patients with normal abdominal clinical measures had dyslipidemia. Self-reported physical activity >30min/day was reported by one third of the patients. No differences were found between physically active and not physically active patients when it came to blood glucose, serum lipid values and clinical measures (paper III). Pain was common in the patient group, however, most often on a mild to moderate level. Anxiety and depression was less common than reported in other studies (paper IV).
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Paulson, Thomas A. W. "Supporting the prescription of exercise in spinal cord injured populations." Thesis, Loughborough University, 2013. https://dspace.lboro.ac.uk/2134/13454.

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Following a spinal cord injury (SCI), participation in regular exercise can enhance physical capacity and performance in activities of daily living. With this in mind, the use of subjective ratings of perceived exertion (RPE) may provide an easy-to-administer alternative to traditional methods of regulating exercise intensity (e.g. heart rate and power output (PO)). A physically active lifestyle is also associated with a reduced risk of cardiovascular disease, in part because exercise exerts anti-inflammatory effects. Examining the plasma response of inflammation-mediating chemical messengers, known as cytokines, to traditional and novel exercise modalities may help maximise the anti-inflammatory potential of regular exercise. Participants with a cervical level SCI successfully self-regulated a 20 min bout of moderate intensity wheelchair propulsion (Chapter three). No differences in physiological or PO responses were observed during the imposed-intensity and self-regulated wheelchair propulsion in the trained population group. In a non-SCI group of novice wheelchair-users, a differentiated RPE specific to the exercising muscle mass (RPEP) was the dominant perceptual signal during submaximal wheelchair propulsion (Chapter four). The novice group successfully self-regulated a 12 min bout of moderate intensity wheelchair propulsion, comprising of a discontinuous 3 x 4 min protocol, using differentiated RPEP. In contrast, a more accurate self-regulation of light intensity wheelchair propulsion was observed when employing traditional overall RPE compared to RPEP. Following strenuous wheelchair propulsion, plasma concentrations of the inflammation-mediating cytokine interleukin-6 (IL-6) were significantly elevated in non-SCI and thoracic level SCI participants (Chapter five). Impaired sympathetic nervous system (SNS) function was associated with a reduced IL-6 response in participants with a cervical level SCI. The plasma IL-6 response to 30 min moderate intensity (60% VO2peak) arm-crank ergometry (ACE) was associated with an elevation in the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra) independent of SNS activation (Chapter six). Light intensity ACE resulted in a small, significant plasma IL-6 response but no IL-1ra response. The addition of functional electrical stimulation-evoked lower-limb cycling to concurrent hand cycling, termed hybrid exercise, resulted in a greater plasma IL-6 response compared to moderate intensity hand cycling alone in participants with a thoracic level SCI (Chapter seven).
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Davies, Diane Susan. "Effects of lifestyle risks on three major disease outcomes in spinal cord injured adults." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22296.pdf.

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Erschbamer, Matthias. "Spinal cord injury : development of protection and repair strategies in rats /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-267-5/.

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López, Serrano Clara. "Role of lysophosphatidic acid receptors in spinal cord injury physiopathology." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458682.

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La médula espinal, la cual constituye una parte vital para el sistema nervioso central (SNC), puede resultar dañada a pesar de estar muy bien protegida por la columna vertebral, dando lugar a importantes consecuencias. La lesión medular provoca una alteración de las redes neuronales que están involucradas en diversas funciones fisiológicas. De hecho, dado que los axones del SNC de mamíferos adultos no pueden regenerarse tras una lesión, y que las células dañadas no pueden ser reparadas, esta patología viene acompañada de una pérdida funcional irreversible para los pacientes afectados. La fisiopatología de la lesión medular se compone de dos fases degenerativas. La fase primaria es consecuencia directa del trauma en la médula, la cual provoca muerte celular, daño axonal y pérdida de mielina. Esta primera fase es sucedida por una secundaria, en la cual se produce un proceso inflamatorio, crucial para el desarrollo de la enfermedad. Aunque la regeneración de los axones dañados y el reemplazo de las neuronas perdidas tras la lesión son objetivos importantes, minimizar el daño secundario a axones, neuronas, mielina y células gliales que sigue al trauma inicial es posiblemente más interesante desde un punto de vista terapéutico. En concreto, la respuesta inflamatoria de esta fase secundaria juega un papel muy importante en la lesión, siendo, por tanto, una buena diana para la búsqueda de una terapia efectiva. Una de las moléculas involucradas en el proceso inflamatorio es el ácido lisofosfatídico (del inglés, LPA), el cual es un lípido bioactivo extracelular que juega un papel importante en diversas funciones fisiológicas. El LPA señaliza a través de seis receptores acoplados a proteína G (LPA1-6), los cuales se clasifican en dos familias: la familia del gen de diferenciación endotelial (del inglés, Edg), que comprende los receptores LPA1-3, y la familia de receptores que no pertenecen a la familia Edg, es decir, Non-Edg (LPA4-6). El LPA se sintetiza a partir de dos vías principales: (i) mediante la acción de la enzima autotaxina (ATX), la cual es la responsable de la síntesis de LPA en plasma, y (ii) mediante la acción de fosfolipasas de tipo de A2 (PLA2), las cuales se encargan de la síntesis en tejido. El LPA juega un papel importante en la fase secundaria de la lesión medular, ya que sus niveles se ven aumentados en el parénquima medular tras el trauma, dando lugar a desmielinización y pérdida de la función locomotora. De hecho, la ausencia de los receptores LPA1 y LPA2 tras la lesión medular mejora la recuperación funcional de los animales y la preservación mielínica en la médula. En esta tesis, revelamos que la activación de los receptores LPA1 y LPA2 microgliales provoca la muerte de los oligodendrocitos. Además, mostramos que los efectos citotóxicos que se desencadenan tras la estimulación de dichos receptores son mediados por la secreción de purinas y la subsecuente activación del receptor P2X7 en oligodendrocitos. Por otro lado, también demostramos que, al contrario de los receptores LPA1 y LPA2, los receptores LPA4 y LPA5 no contribuyen a la fisiopatología de la lesión medular. En el presente trabajo, también mostramos que la inhibición farmacológica de la ATX no tiene ningún efecto en la recuperación funcional ni el daño secundario tras la lesión medular, lo cual sugiere que la fuente principal de LPA en esta patología no es la síntesis en plasma. Además, demostramos que el bloqueo combinado de LPA1 y LPA2 no tiene efectos aditivos en la lesión medular. En general, los resultados de esta tesis sugieren que la inhibición farmacológica del LPA1 y, preferiblemente el LPA2, abren una nueva ventana terapéutica para el tratamiento de la lesión medular
The spinal cord is an extremely vital part of the central nervous system (CNS) and, although it is well protected by the spinal column, it can be damaged, resulting in serious consequences. Spinal cord injury (SCI) leads to a disruption of the neuronal networks that are involved in many physiological functions. Since CNS axons of adult mammals do not regenerate following the lesion, and dead neurons and glial cells are not successfully replaced, this results in an irreversible functional loss in patients suffering from SCI. The pathophysiology of SCI involves two degenerative stages, known as primary and secondary injury. The first one results from the direct mechanical trauma to the spinal cord, directly causing cell death, damage to axons, and loss of myelin. This is followed by a secondary wave of tissue degeneration that can extend for several weeks, in which inflammation plays a crucial role. Although regeneration of damaged axons and replacement of lost neurons and glial cells are important goals for the restoration of the injured spinal cord, minimizing secondary damage to axons, neuronal cell bodies, myelin and glial cells that follows the initial trauma is likely to be more easily amenable to treatment. Since inflammation is a major contribution to secondary damage in SCI, targeting the detrimental actions of this physiological response could result in the development of novel approaches for the treatment of this pathology. Lysophosphatidic acid (LPA) is an extracellular bioactive lipid with many physiological functions. It signals through six known G-protein coupled receptors (LPA1-6), which are classified into two families: Endothelial differentiation family gene (Edg) LPA receptors (LPA1-3) and Non-Edg family gene LPA receptors (LPA4-6). LPA synthesis is carried out by two different pathways: (i) by the action of the enzyme named autotaxin (ATX), which is the main responsible in synthesis of this lipid in plasma, and (ii) by action of the phospholipase A2 (PLA2) family enzymes, which are the main route of LPA synthesis in tissues. LPA is a key trigger of secondary damage after SCI, since its increased levels in the spinal cord parenchyma following injury leads to demyelination. Indeed, the lack of LPA1 and LPA2 signalling after SCI enhances functional recovery and myelin sparing. In this thesis, we show that activation of microglial LPA1 and LPA2 leads to oligodendrocyte cell death. We reveal that the cytotoxic actions underlying by microglial cells stimulated with LPA are mediated by the release of purines and the subsequent activation of P2X7 in oligodendrocytes. We also show that, unlike LPA1 and LPA2, LPA4 and LPA5 receptors do not contribute to SCI physiopathology. In the present thesis, we also show that pharmacological inhibition of ATX does not have any effect in functional outcomes and secondary tissue damage after SCI, suggesting that this enzyme is unlikely to be involved in the production of LPA in the spinal cord parenchyma after injury. We also demonstrate that combinatory targeting of LPA1 and LPA2 does not results in additive effects in SCI. Overall, the results shown here suggest that pharmacological inhibition of LPA1, and preferably LPA2, may open a new therapeutic avenue for the treatment of SCI.
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Pahuta, Markian. "Decision Analysis of Surgical Treatment Indications for Metastatic Epidural Spinal Cord Compression." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39390.

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Metastatic epidural spinal cord compression (MESCC) occurs when tumour invades the epidural space and compresses the spinal cord. Despite Level 1 evidence that surgery is the most effective treatment for MESCC, there is controversy regarding the role of surgery because of fear that patients who have a short survival will spend a large fraction of their remaining life recovering from surgery and potential complications. This controversy could be resolved by decision-analysis of MESCC treatments using quality-adjusted-life-years (QALYs). There have been two barriers to conducting decision-analysis of QALYs for MESCC: (a) lack of utility data, and (b) skepticism regarding decision-analysis. The first four research chapters in this thesis address these barriers. The final research chapter reports a decision-analysis of QALYs on the role of surgery in MESCC. Chapter 1 provides background information on the controversy regarding surgical treatment for MESCC and the rationale for each of the subsequent chapters. Chapter 2 reports a psychometric validation study of a web-based utility valuation module for MESCC. In Chapter 3, application of this module to a general population utility valuation study with a market research panel is described. In Chapter 4, the beneficial properties of Bayesian statistical analysis to minimizing “arbitrariness” in probabilistic sensitivity analysis are described in relation to prognostication for MESCC. Chapter 5 presents a strategy for simplifying and enhancing the transparency of Markov cohort simulation. Finally, the work presented in the research chapters is applied in Chapter 6 to conduct Markov cohort simulation to determine if patients with short survival derive net health-related quality-of-life benefit from surgery. Pragmatic research around barriers to decision-analysis of QALYs for MESCC was conducted to resolve the controversy regarding the role of surgery in the treatment of MESCC. Under most circumstances, MESCC patients who can ambulate prior to treatment derive net HRQoL benefit from surgery, even if prognosis is poor. Non-ambulatory patients can derive net HRQoL benefit but only if the morbidity of surgery is relatively low. It is my hope that the work used to address barriers to decision-analysis of QALYs will be disseminated and applied in other clinical problems.
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Cooper, Cindy L. "Neuropeptides, amines and amine receptors in the human spinal cord : the effects of Parkinson's disease." Thesis, University of Nottingham, 1989. http://eprints.nottingham.ac.uk/13218/.

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The aims of this study were to investigate (i) the levels of catecholamines, indoleamines, substance P and thyrotrophin-releasing hormone (TRH) in the post-mortem spinal cord of subjects who had died with Parkinson's disease and to compare them with those of control subjects (ii) adrenergic and serotonergic receptors in the post-mortem Parkinsonian and control spinal cord and (iii) the effects of subject age and sex and the interval between death and post-mortem (PMI) on the levels of neurotransmitters and neuropeptides and on receptor binding in post-mortem tissue. To perform these investigations (i) a sensitive radioimmunoassay which is specific for substance P and has low cross-reactivity with other similar peptides and (ii) a common extraction medium for the concomitant extraction of catecholamines, indoleamines, substance P and TRH from CNS tissue were developed. The main findings were: There were significant correlations between the levels of 5HT, TRH and α2-adrenoceptor binding and both subject age and the PMI. In Parkinson's disease compared with control subjects: (i) the levels of noradrenaline were significantly reduced in the thoracic ventral region of the spinal cord,(ii) dopamine levels were higher in the thoracic ventral and dorsal spinal cord,(iii) in the lumbar spinal cord 5HT levels were significantly reduced in the dorsal horn with an increase in the ratio of 5HIAA/5HT, (iv) noradrenaline levels were reduced in both dorsal and ventral horns of the lumbar spinal cord and (v) there were no differences between the levels of substance P and TRH in any spinal cord region. There were no measurable 5HT1A or 5HT2 binding sites in the human spinal cord under the conditions used. However, specific α2-adrenoceptor binding was defined in terms of binding affinity and number of receptors in the spinal cord.
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Books on the topic "Spinal cord disease"

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Critchley, Edmund, Andrew Eisen, and Michael Swash, eds. Spinal Cord Disease. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5.

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Critchley, Edmund, and Andrew Eisen, eds. Spinal Cord Disease. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2.

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Consortium for Spinal Cord Medicine. Acute management of autonomic dysreflexia: Individuals with spinal cord injury presenting to health-care facilities. 2nd ed. Washington, DC: Consortium for Spinal Cord Medicine, 2001.

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1953-, Marks Michael P., and Do Huy M, eds. Endovascular and percutaneous therapy of the brain and spine. Philadelphia: Lippincott Williams & Wilkins, 2002.

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G, Waxman Stephen, ed. Molecular and cellular approaches to the treatment of neurological disease. New York: Raven Press, 1993.

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D, Bartleson J., and Deen H. Gordon, eds. Spine disorders: Medical and surgical management. Cambridge: Cambridge University Press, 2009.

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Parker, James N., and Philip M. Parker. Sandhoff disease: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. San Diego, CA: ICON Health Publications, 2007.

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R, Critchley E. M., and Eisen Andrew 1936-, eds. Diseases of the spinal cord. London: Springer-Verlag, 1992.

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LeCouteur, Richard. Diseases of the spinal cord. Sydney South, NSW, Australia: Post Graduate Committee in Veterinary Science, University of Sydney, 1991.

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Critchley, Edmund, and Andrew Eisen, eds. Diseases of the Spinal Cord. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3353-7.

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Book chapters on the topic "Spinal cord disease"

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Gurusinghe, N. T. "Spinal Tumours." In Spinal Cord Disease, 501–43. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2_30.

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Gurusinghe, N. T. "Spinal Tumours." In Spinal Cord Disease, 501–43. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5_30.

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Eisen, A. A. "Radiculopathy due to Diseases other than Disc Disease." In Spinal Cord Disease, 203–17. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2_12.

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Eisen, A. A. "Radiculopathy due to Diseases other than Disc Disease." In Spinal Cord Disease, 203–17. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5_12.

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Jacobson, Ryan, and Allison Osen. "Spinal Cord Disease." In Hankey's Clinical Neurology, 717–48. Third edition. | Boca Raton ; London : CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9780429299476-23.

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Arnold, Susan, Heidi Barnes Heller, Joy Delamaide Gasper, and Julien Guevar. "Spinal Cord Disease." In Small Animal Neuroanatomic Lesion Localization Practice Book, 62–106. GB: CABI, 2022. http://dx.doi.org/10.1079/9781789247947.0005.

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Aminoff, M. J. "Spinal Vascular Disease." In Spinal Cord Disease, 423–42. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2_24.

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Aminoff, M. J. "Spinal Vascular Disease." In Spinal Cord Disease, 423–42. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5_24.

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Dick, J. P. R. "Spinal Epidural Abscess." In Spinal Cord Disease, 495–99. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0911-2_29.

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Dick, J. P. R. "Spinal Epidural Abscess." In Spinal Cord Disease, 495–99. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0569-5_29.

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Conference papers on the topic "Spinal cord disease"

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Muniz Veloso, Leila Patrícia, Claudia Lopes Santoro Neiva, Lilian Santuza Santos Porto, and Fernanda Armond Castro. "SARCOIDOSIS WITH BONE AND SPINAL CORD INVOLVEMENT MIMICKING METASTATIC DISEASE." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17428.

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Brum, Igor Vilela, Guilherme Diogo Silva, Diego Sant'Ana Sodre, Felipe Melo Nogueira, Samira Luisa dos Apostolos Pereira, and Luiz Henrique Martins Castro. "Myelopathy in sickle cell disease: a case-oriented review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.563.

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Background: Although neurological complications are well recognized in sickle cell disease (SCD), myelopathy has been rarely described. We present the first case report of longitudinally extensive myelitis (LETM) in SCD and review the differential diagnosis of myelopathy in these patients. Design and setting: case-oriented review. Methods: We report the case of a 29-year-old African-Brazilian man with SCD, who experienced a subacute flaccid paraparesis, with T2 sensory level and urinary retention. CSF analysis showed a lymphocytic pleocytosis and increased protein levels. MRI disclosed a longitudinally extensive spinal cord lesion, with a high T2/STIR signal extending from C2 to T12. Serum anti-aquaporin-4 antibody was negative. We searched Medline/ PubMed, Embase, Scopus, and Google Scholar databases for myelopathy in SCD patients. Results: Spinal cord compression by vertebral fractures, extramedullary hematopoietic tissue, and Salmonella epidural abscess have been reported in SCD. We found only three case reports of spinal cord infarction, which is unexpectedly infrequent compared to the prevalence of cerebral infarction in SCD. We found only one case report of varicella-zoster myelitis and no previous report of LETM in SCD patients. Conclusion: Specific and time-sensitive causes of myelopathy should be considered in SCD patients. In addition to compression and ischemia, LETM should be considered as a possible mechanism of spinal cord involvement in SCD.
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Marin, Carolina Maria, Gustavo Carvalho Costa, Emilia Correa Souto, Icaro França Navarro Pinto, Igor Braga Farias, Bruno de Mattos Lombardi Badia, Roberta Ismael Lacerda Machado, Paulo Victor Sgobbi Souza, Wladimir Bocca Vieira de Rezende Pinto, and Acary Souza Bulle Oliveira. "Charcot arthropathy in the elbow caused by hydrosiringomyelia." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.148.

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Introduction: Syringomyelia is a chronic disease of the spinal cord that leads to damage to nerve fibers in the spinothalamic tract. The changes in these structures responsible for the thermal and painful sensitivity lead to an abnormal innervation of the joints, which can lead to neuropathic arthropathy, called Charcot arthropathy. Syringomyelia is the main cause of Charcot arthropathy in the upper limbs, and the most involving joints are the shoulder and elbow. It is a rare condition and its recognition allows for early diagnosis and proper management. Case report: A 50-year-old female patient, with a previous history of spinal cord trauma, who has been in a wheelchair since then, started with edema in the left upper limb, mainly in the elbow, evolved with local ulcer and presence of serosanguinolent secretion, weakness and paresthesia in the left hand. Magnetic resonance imaging of the elbow showed signs of neuroarthropathy and the study of the thoracic cervical spine showed enlargement of the cerebrospinal fluid space and tapering of the spinal cord. Conclusions: Charcot’s arthropathy should be considered as a differential diagnosis of pain, edema and limitation of joint movements. When present in the upper limbs, an investigation should be carried out to exclude syringomyelia.
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Liu, Yifei, Bryn A. Martin, Thomas J. Royston, and Francis Loth. "A Fluid Structure Interaction Simulation of the Cerebrospinal Fluid, Spinal Cord, and Spinal Stenosis Present in Syringomyelia." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19433.

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Syringomyelia (SM) is a neurological disease in which a fluid-filled cystic cavity, or syrinx, forms in the spinal cord (SC) resulting in progressive loss of sensory, motor functions, and/or pain in the patient. It has been hypothesized that abnormal cerebrospinal fluid (CSF) pressure distribution and absorption in the subarachnoid space (SAS), resulting from a CSF flow blockage (stenosis), could be a key etiological factor for syrinx pathogenesis. In particular, the magnitude of the abrupt SAS pressure waves produced during coughing has been correlated with headache and pain in the patient. To better understand the influence of coughing on the spinal SAS, four axisymmetric fluid-structure interaction (FSI) in silico models representative of various conditions associated with SM were constructed. Each of the models was subjected to a cough-like CSF pressure pulse. The CSF flow stenosis was shown to attenuate and decelerate the CSF wave propagation in the SAS. The spinal SAS distensibility was also shown to have significant influence on the wave propagation. The in silico pressure results were found to be in agreement with a set of similar in vitro experiments [1].
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Elliott, Novak S. J., Anthony D. Lucey, Duncan A. Lockerby, and Andrew R. Brodbelt. "Syringomyelia and the Fluid-Structure Interactions of a Cerebrospinal Waveguide." In ASME 2014 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/pvp2014-29095.

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In the disease syringomyelia, fluid-filled cavities, called syrinxes, form in the spinal cord. The expansion of these pathological pressure vessels compresses the surrounding nerve fibers and blood supply, which is associated with neurological damage. We investigate the spinal wave-propagation characteristics, principally to serve as a reference for more anatomically-detailed models. The spinal cord is modeled as an elastic cylinder, which becomes an annulus containing inviscid fluid when a syrinx is included. This is surrounded by an annulus of inviscid fluid, representing the cerebrospinal fluid occupying the subarachnoid space, with an outer rigid boundary approximating the dura mater. The axisymmetric harmonic motion is solved as an eigenvalue problem. We present dispersion diagrams and describe the physical mechanism of each wave mode. We identify potentially damaging syrinx fluid motions and tissue stress concentrations from the eigenvectors. Finally, we determine the dependence of each wave mode on syrinx radius and cord tissue compressibility.
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Dias, Mariana de Souza, and Matheus Felipe de Souza Vasconcelos. "Conus medullaris syndrome caused by spinal cord schistosomiasis: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.529.

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Background: Neuroschistosomiasis is a rare but severe complication of schistosomiasis that is often underdiagnosed and can affect both the brain and the spinal cord. CNS involvement occurs during hepato-intestinal or intestinal phase of the disease, when the Schistosoma eggs or adult worms reach the vertebral venous plexuses via Batson plexuses. Objective: To report a case of a patient with conus medullaris syndrome caused by spinal cord schistosomiasis whose symptoms had great improvement after undergoing treatment with praziquantel and prednisone. Case report: A 45-year-old woman, from Bahia, Brazil, with no significant medical history, presented with intense pain in her legs from knees below, associated with progressive loss of strength, tingling and dysesthesias in both lower limbs, causing gait impairment followed by urinary retention. At physical examination, grade III paraparesis in proximal limbs and grade IV in distal limbs and unsteady dysbasic gait were observed, no meningeal signs were found. MRI study revealed hyperintense signal in medulla at the level of T12-L1 to conus medullaris in T2 sequences, mainly on central portions and medulla, also slight impregnation with gadolinium showing dotted pattern was observed, suggestive findings of inflammatory myelitis. KatoKatz test was performed evidencing Schistosoma eggs. After diagnosis, patient was treated with prednisone and praziquantel for 5 weeks. At the end the of treatment, she has showed progressive improvement of her symptoms. In our last evaluation, the patient showed a great recovery of movement and strength, now grade IV in proximal limbs and grade V in distal limbs as well as a steadier gait. Urinary retention is still present, and she still needs intermittent catheterization for the time being Conclusion: Neuroschistosomiasis, when symptomatic, is a severe disorder in which can cause significant incapacity and morbidity. It is an underdiagnosed disorder but has been increasingly reported in populations in endemic areas and in tourists. Prognosis depends largely on early diagnosis and treatment.
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Ferrari Bardile, Costanza, Harwin Sidik, Reynard Quek, Nur Amirah Binte Mohammad Yusof, Marta Garcia-Miralles, and Mahmoud A. Pouladi. "A13 Abnormal spinal cord myelination due to oligodendrocyte dysfunction in a model of huntington disease." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.12.

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Gloeckner, D. Claire, Michael B. Chancellor, and Michael S. Sacks. "Changes in Material Classification of the Urinary Bladder Wall After Spinal Cord Injury." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32523.

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Changes in the mechanical properties of the urinary bladder wall following neurogenic disease or trauma can result in bladder dysfunction. We have recently reported changes in the biaxial mechanical properties of the bladder wall 10 days after spinal cord injury in a rat model [1]. Development of a constitutive model to characterize these changes would facilitate quantitative comparisons and provide the necessary information for organ-level computational modeling. However, before an appropriate constitutive model of the bladder wall can be formulated, its material class must be identified. In the present study, we applied a generalized method for material classification of biaxial mechanical data to our previous data on the urinary bladder wall.
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Pires, Bianca Frigo, and Osmi Hamamoto. "Serological screening for syphilis in non-compressive spinal injuries." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.117.

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Background: Syphilis is an infectious disease that can present systemic symptoms during its progression, reaching the central nervous system, causing neurosyphilis, combined include involvement of the meninges and spinal cord. Objectives: to review information on meningomyelitis in patients with positive syphilis serology, assessing the need for serological screening for syphilis knowledge and the importance of the clinician for an accurate diagnosis, preventing major sequelae or fatalities Methods: We analyzed 14 clinical cases of syphilitic myelitis from January 2000 to January 2021. Documents were resolved to determine clinical issues, apparent symptoms, radiological findings, penal treatment and complications. Results: 85.7% suffered from chronic myelopathy and 14.3% revealed subacute transverse myelitis. The most common clinical condition of chronic myelopathy was tabes dorsalis, present in 50%, afterwards it was syphilitic meningomyelite, present in 33.3%. Conclusion: Syphilitic myelitis is a rare condition, but there are studies that prove an increase in cases of myelopathy in patients with positive syphilis serology. The condition manifests itself with weakness of the lower limbs, sensory disturbance and urinary and fecal incontinence, in addition to long spinal cord injuries and abnormal enhancement, predominantly in the superficial parts of the spinal cord, in imaging exams. There is a differential diagnosis with multiple pathologies, such as intramedullary tumors, herniated intervertebral disc, myelopathy caused by HIV, among others. Therefore, it is important to know the signs and symptoms and an approach to serological screening for syphilis in patients with neurological disorders and non-compressive medical injuries.
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Borges, Matheus Araújo, Isabel Cristina Borges de Menezes, Isabela Garcia Bessa, Gabrielly de Souza Correia, Maria Clara Rocha Elias Dib, Rafaela Joy Falcão, and Leslivan Ubiratan Moraes. "Sexual dysfunction associated with neurological disorders in men aged 19 to 44 years." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.164.

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Introduction: Male sexual dysfunction (DSM) is characterized by changes in qualitative or quantitative sexual capacity, manifested by changes in ejaculation, erection, and/or orgasm, in addition to the presence of pain or discomfort in sexual relations, and the main one of these is erectile dysfunction (ED). Objective: Review the literature on sexual dysfunction caused by neurological disorders, in men aged 19 to 44 years. Methodology: This is a narrative literature review. The collection of information about the theme was carried out through a search for scientific articles in the PubMed databases. The descriptions used in the search were “sexual dysfunction AND neurological disorders in men”, articles published in the last 5 years were considered. Results: Several neurological diseases with a very high correlation with DSM were found, such as: multiple sclerosis, ED being the main problem reported by patients, depression and its respective treatment, epilepsy, mainly associated with anxiety and depression, Parkinson’s disease, spinal cord injury, spina bifida, stroke and traumatic brain injury, especially when associated with diabetic neuropathy. Conclusion: DS is a very frequent problem in neurological diseases, therefore, there is a need for this theme not to be neglected by health professionals, emphasizing the importance of multidisciplinary treatment. Mersh Terms: Impotence, Male Sexual Impotence, Nervous System Disease.
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Reports on the topic "Spinal cord disease"

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Zhu, Zhihong, Yue Zhuo, Haitao Jin, Boyu Wu, and Zhijie Li. Chinese Medicine Therapies for Neurogenic Bladder after Spinal Cord Injury: A protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0084.

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Neurogenic bladder (NB), a refractory disease, is characterized by voiding dysfunction of bladder and/or urethra, and spinal cord injury (SCI) is a common cause. Chinese medicine therapies have been applied extensively in the treatment of neurogenic bladder, especially in China, and the results are promising but varying. Thus, the aim of this work is to assess the efficacy and safety of various Chinese medicine therapies for neurogenic bladder after spinal cord injury. Condition being studied: Chinese medicine therapies; Neurogenic bladder after spinal cord injury. Main outcome(s): The primary outcome of our NMA will be measured by overall response rate and urodynamic tests, which includes postvoiding residual urine volume, maximum urinary flow rate, and maximal detrusor pressure.
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Yang, Xinwei, Huan Tu, and Xiali Xue. The improvement of the Lower Limb exoskeletons on the gait of patients with spinal cord injury: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0095.

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Review question / Objective: The purpose of this systematic review and meta-analysis was to determine the efficacy of lower extremity exoskeletons in improving gait function in patients with spinal cord injury, compared with placebo or other treatments. Condition being studied: Spinal Cord Injury (SCI) is a severely disabling disease. In the process of SCI rehabilitation treatment, improving patients' walking ability, improving their self-care ability, and enhancing patients' self-esteem is an important aspect of their return to society, which can also reduce the cost of patients, so the rehabilitation of lower limbs is very important. The lower extremity exoskeleton robot is a bionic robot designed according to the principles of robotics, mechanism, bionics, control theory, communication technology, and information processing technology, which can be worn on the lower extremity of the human body and complete specific tasks under the user's control. The purpose of this study was to evaluate the effect of the lower extremity exoskeleton on the improvement of gait function in patients with spinal cord injury.
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Zhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao, and Gang Chen. Risk factors associated with amyotrophic lateral sclerosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.

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Review question / Objective: To identify and list the risk factors associated with the onset and progression of ALS. Condition being studied: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting the upper and lower motor neurons in the spinal bulb, cerebral cortex, and spinal cord. The clinical processing symptoms accompany muscle atrophy, fasciculation, and fatigue of limbs, which can lead to general paralysis and death from respiratory failure within 3-5 years after the onset of this disease. Though the pathogenesis of ALS is still unclear, exploring the associations between risk factors and ALS can provide reliable evidence to find the pathogenesis in the future. This meta-analysis aims to synthesize all related risk factors on ALS, comprehensively understand this disease, and provide clues to mechanism research and clinicians.
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Selph, Shelly S., Andrea C. Skelly, Ngoc Wasson, Joseph R. Dettori, Erika D. Brodt, Erik Ensrud, Diane Elliot, et al. Physical Activity and the Health of Wheelchair Users: A Systematic Review in Multiple Sclerosis, Cerebral Palsy, and Spinal Cord Injury. Agency for Healthcare Research and Quality (AHRQ), October 2021. http://dx.doi.org/10.23970/ahrqepccer241.

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Objectives. Although the health benefits of physical activity are well described for the general population, less is known about the benefits and harms of physical activity in people dependent upon, partially dependent upon, or at risk for needing a wheelchair. This systematic review summarizes the evidence for physical activity in people with multiple sclerosis, cerebral palsy, and spinal cord injury regardless of current use or nonuse of a wheelchair. Data sources. We searched MEDLINE®, CINAHL®, PsycINFO®, Cochrane CENTRAL, Embase®, and Rehabilitation and Sports Medicine Source from 2008 through November 2020, reference lists, and clinical trial registries. Review methods. Predefined criteria were used to select randomized controlled trials, quasiexperimental nonrandomized trials, and cohort studies that addressed the benefits and harms of observed physical activity (at least 10 sessions on 10 different days of movement using more energy than rest) in participants with multiple sclerosis, cerebral palsy, and spinal cord injury. Individual study quality (risk of bias) and the strength of bodies of evidence for key outcomes were assessed using prespecified methods. Dual review procedures were used. Effects were analyzed by etiology of impairment and physical activity modality, such as treadmill, aquatic exercises, and yoga, using qualitative, and when appropriate, quantitative synthesis using random effects meta-analyses. Results. We included 146 randomized controlled trials, 15 quasiexperimental nonrandomized trials, and 7 cohort studies (168 studies in 197 publications). More studies enrolled participants with multiple sclerosis (44%) than other conditions, followed by cerebral palsy (38%) and spinal cord injury (18%). Most studies were rated fair quality (moderate risk of bias). The majority of the evidence was rated low strength. • In participants with multiple sclerosis, walking ability may be improved with treadmill training and multimodal exercise regimens that include strength training; function may be improved with treadmill training, balance exercises, and motion gaming; balance is likely improved with postural control exercises (which may also reduce risk of falls) and may be improved with aquatic exercises, robot-assisted gait training, treadmill training, motion gaming, and multimodal exercises; activities of daily living may be improved with aquatic therapy; sleep may be improved with aerobic exercises; aerobic fitness may be improved with multimodal exercises; and female sexual function may be improved with aquatic exercise. • In participants with cerebral palsy, balance may be improved with hippotherapy and motion gaming, and function may be improved with cycling, treadmill training, and hippotherapy. • In participants with spinal cord injury, evidence suggested that activities of daily living may be improved with robot-assisted gait training. • When randomized controlled trials were pooled across types of exercise, physical activity interventions were found to improve walking in multiple sclerosis and likely improve balance and depression in multiple sclerosis. Physical activity may improve function and aerobic fitness in people with cerebral palsy or spinal cord injury. When studies of populations with multiple sclerosis and cerebral palsy were combined, evidence indicated dance may improve function. • Evidence on long-term health outcomes was not found for any analysis groups. For intermediate outcomes such as blood pressure, lipid profile, and blood glucose, there was insufficient evidence from which to draw conclusions. There was inadequate reporting of adverse events in many trials. Conclusions. Physical activity was associated with improvements in walking ability, general function, balance (including fall risk), depression, sleep, activities of daily living, female sexual function, and aerobic capacity, depending on population enrolled and type of exercise utilized. No studies reported long-term cardiovascular or metabolic disease health outcomes. Future trials could alter these findings; further research is needed to examine health outcomes, and to understand the magnitude and clinical importance of benefits seen in intermediate outcomes.
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Zheng, Ruo-xiang, Jia-wei Xu, Bi-yao Jiang, Wei Tang, Chun-li Lu, Xiao-yang Hu, and Jian-ping Liu. Mind-body therapies in traditional Chinese medicine for neuropathic pain: a systematic review of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0016.

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Review question / Objective: The purpose of this review is to comprehensively evaluate the effectiveness and safety on mind-body therapies of traditional Chinese medicine for neuropathic pain. Condition being studied: According to the definition by the International Association for the Study of Pain (IASP), neuropathic pain is a kind of pain caused by lesions or diseases affecting the somatosensory nervous system. It has brought considerable negative impacts on patients and society. Neuropathic pain is a prevalent disease and can be induced by a variety of clinical conditions such as spinal cord injury (prevalence rate: 53%), induced peripheral neuropathic pain (prevalence rate: 38%), diabetic peripheral neuropathic pain (prevalence rate: 10%-26%), chemotherapy postherpetic neuralgia (3.9-42.0/10,000 people per year), prosopalgia (3-5/10,000 people per year), and so on. However, current recommended medicines for neuropathic pain management could cause dependence and adverse events. Thus, alternatives would be helpful for both patients and clinicians. Mind-body therapy in traditional Chinese medicine (TCM) has a long history in clinical practice for relieving pain and their effectiveness has not been systematically reviewed.The purpose of this review is to comprehensively evaluate the effectiveness and safety on mind-body therapies of traditional Chinese medicine for neuropathic pain.
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Newman-Toker, David E., Susan M. Peterson, Shervin Badihian, Ahmed Hassoon, Najlla Nassery, Donna Parizadeh, Lisa M. Wilson, et al. Diagnostic Errors in the Emergency Department: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2022. http://dx.doi.org/10.23970/ahrqepccer258.

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Objectives. Diagnostic errors are a known patient safety concern across all clinical settings, including the emergency department (ED). We conducted a systematic review to determine the most frequent diseases and clinical presentations associated with diagnostic errors (and resulting harms) in the ED, measure error and harm frequency, as well as assess causal factors. Methods. We searched PubMed®, Cumulative Index to Nursing and Allied Health Literature (CINAHL®), and Embase® from January 2000 through September 2021. We included research studies and targeted grey literature reporting diagnostic errors or misdiagnosis-related harms in EDs in the United States or other developed countries with ED care deemed comparable by a technical expert panel. We applied standard definitions for diagnostic errors, misdiagnosis-related harms (adverse events), and serious harms (permanent disability or death). Preventability was determined by original study authors or differences in harms across groups. Two reviewers independently screened search results for eligibility; serially extracted data regarding common diseases, error/harm rates, and causes/risk factors; and independently assessed risk of bias of included studies. We synthesized results for each question and extrapolated U.S. estimates. We present 95 percent confidence intervals (CIs) or plausible range (PR) bounds, as appropriate. Results. We identified 19,127 citations and included 279 studies. The top 15 clinical conditions associated with serious misdiagnosis-related harms (accounting for 68% [95% CI 66 to 71] of serious harms) were (1) stroke, (2) myocardial infarction, (3) aortic aneurysm and dissection, (4) spinal cord compression and injury, (5) venous thromboembolism, (6/7 – tie) meningitis and encephalitis, (6/7 – tie) sepsis, (8) lung cancer, (9) traumatic brain injury and traumatic intracranial hemorrhage, (10) arterial thromboembolism, (11) spinal and intracranial abscess, (12) cardiac arrhythmia, (13) pneumonia, (14) gastrointestinal perforation and rupture, and (15) intestinal obstruction. Average disease-specific error rates ranged from 1.5 percent (myocardial infarction) to 56 percent (spinal abscess), with additional variation by clinical presentation (e.g., missed stroke average 17%, but 4% for weakness and 40% for dizziness/vertigo). There was also wide, superimposed variation by hospital (e.g., missed myocardial infarction 0% to 29% across hospitals within a single study). An estimated 5.7 percent (95% CI 4.4 to 7.1) of all ED visits had at least one diagnostic error. Estimated preventable adverse event rates were as follows: any harm severity (2.0%, 95% CI 1.0 to 3.6), any serious harms (0.3%, PR 0.1 to 0.7), and deaths (0.2%, PR 0.1 to 0.4). While most disease-specific error rates derived from mainly U.S.-based studies, overall error and harm rates were derived from three prospective studies conducted outside the United States (in Canada, Spain, and Switzerland, with combined n=1,758). If overall rates are generalizable to all U.S. ED visits (130 million, 95% CI 116 to 144), this would translate to 7.4 million (PR 5.1 to 10.2) ED diagnostic errors annually; 2.6 million (PR 1.1 to 5.2) diagnostic adverse events with preventable harms; and 371,000 (PR 142,000 to 909,000) serious misdiagnosis-related harms, including more than 100,000 permanent, high-severity disabilities and 250,000 deaths. Although errors were often multifactorial, 89 percent (95% CI 88 to 90) of diagnostic error malpractice claims involved failures of clinical decision-making or judgment, regardless of the underlying disease present. Key process failures were errors in diagnostic assessment, test ordering, and test interpretation. Most often these were attributed to inadequate knowledge, skills, or reasoning, particularly in “atypical” or otherwise subtle case presentations. Limitations included use of malpractice claims and incident reports for distribution of diseases leading to serious harms, reliance on a small number of non-U.S. studies for overall (disease-agnostic) diagnostic error and harm rates, and methodologic variability across studies in measuring disease-specific rates, determining preventability, and assessing causal factors. Conclusions. Although estimated ED error rates are low (and comparable to those found in other clinical settings), the number of patients potentially impacted is large. Not all diagnostic errors or harms are preventable, but wide variability in diagnostic error rates across diseases, symptoms, and hospitals suggests improvement is possible. With 130 million U.S. ED visits, estimated rates for diagnostic error (5.7%), misdiagnosis-related harms (2.0%), and serious misdiagnosis-related harms (0.3%) could translate to more than 7 million errors, 2.5 million harms, and 350,000 patients suffering potentially preventable permanent disability or death. Over two-thirds of serious harms are attributable to just 15 diseases and linked to cognitive errors, particularly in cases with “atypical” manifestations. Scalable solutions to enhance bedside diagnostic processes are needed, and these should target the most commonly misdiagnosed clinical presentations of key diseases causing serious harms. New studies should confirm overall rates are representative of current U.S.-based ED practice and focus on identified evidence gaps (errors among common diseases with lower-severity harms, pediatric ED errors and harms, dynamic systems factors such as overcrowding, and false positives). Policy changes to consider based on this review include: (1) standardizing measurement and research results reporting to maximize comparability of measures of diagnostic error and misdiagnosis-related harms; (2) creating a National Diagnostic Performance Dashboard to track performance; and (3) using multiple policy levers (e.g., research funding, public accountability, payment reforms) to facilitate the rapid development and deployment of solutions to address this critically important patient safety concern.
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