Journal articles: '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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Augustinsson, Lars E., Bengt Linderoth, Clas Mannheimer, and Tore Eliasson. "Spinal Cord Stimulation in Cardiovascular Disease." Neurosurgery Clinics of North America 6, no. 1 (January 1995): 157–65. http://dx.doi.org/10.1016/s1042-3680(18)30484-4.

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Kamin, Stephen, and Susan Garstang. "Vascular Disease of the Spinal Cord." Topics in Spinal Cord Injury Rehabilitation 14, no. 2 (October 2008): 42–52. http://dx.doi.org/10.1310/sci1402-42.

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Pace, A. V. "Spinal cord stimulation in Buerger's disease." Annals of the Rheumatic Diseases 61, no. 12 (December 1, 2002): 1114. http://dx.doi.org/10.1136/ard.61.12.1114.

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Bartley, Paul P., Michael P. Pender, Marion L. Woods, Duncan Walker, James A. Douglas, Anthony M. Allworth, Damon P. Eisen, and Bart J. Currie. "Spinal cord disease due to melioidosis." Transactions of the Royal Society of Tropical Medicine and Hygiene 93, no. 2 (March 1999): 175–76. http://dx.doi.org/10.1016/s0035-9203(99)90299-7.

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Stewart, Randolph H., and Joyce P. Grzffiths. "Medical Management of Spinal Cord Disease." Veterinary Clinics of North America: Equine Practice 3, no. 2 (August 1987): 429–36. http://dx.doi.org/10.1016/s0749-0739(17)30685-5.

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Longo, Walter E., Garth H. Ballantyne, and Irvin M. Modlin. "Colorectal disease in spinal cord patients." Diseases of the Colon & Rectum 33, no. 2 (February 1990): 131–34. http://dx.doi.org/10.1007/bf02055542.

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Crichton, J. H. "ACUTE SPINAL CORD DISEASE IN CHILDHOOD." Developmental Medicine & Child Neurology 23, no. 6 (November 12, 2008): 643–46. http://dx.doi.org/10.1111/j.1469-8749.1981.tb02046.x.

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Kolos, Elena, and Dmitry Korzhevsky. "Spinal cord microglia in health and disease." Acta Naturae 12, no. 1 (April 16, 2020): 4–17. http://dx.doi.org/10.32607/actanaturae.10934.

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The review summarizes data of recent experimental studies on spinal microglia, the least explored cells of the spinal cord. It focuses on the origin and function of microglia in mammalian spinal cord embryogenesis. The main approaches to the classification of microgliocytes based on their structure, function, and immunophenotypic characteristics are analyzed. We discuss the results of studies conducted on experimental models of spinal cord diseases such as multiple sclerosis, amyotrophic lateral sclerosis, systemic inflammation, and some others, with special emphasis on the key role of microglia in the pathogenesis of these diseases. The review highlights the need to detect the new microglia-specific marker proteins expressed at all stages of ontogeny. New sensitive and selective microglial markers are necessary in order to improve identification of spinal cord microgliocytes in normal and pathological conditions. Possible morphometric methods to assess the functional activity of microglial cells are presented.

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Tsagkas, Charidimos, Stefano Magon, Laura Gaetano, Simon Pezold, Yvonne Naegelin, Michael Amann, Christoph Stippich, et al. "Spinal cord volume loss." Neurology 91, no. 4 (June 27, 2018): e349-e358. http://dx.doi.org/10.1212/wnl.0000000000005853.

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ObjectiveCross-sectional studies have shown that spinal cord volume (SCV) loss is related to disease severity in multiple sclerosis (MS). However, long-term data are lacking. Our aim was to evaluate SCV loss as a biomarker of disease progression in comparison to other MRI measurements in a large cohort of patients with relapse-onset MS with 6-year follow-up.MethodsThe upper cervical SCV, the total brain volume, and the brain T2 lesion volume were measured annually in 231 patients with MS (180 relapsing-remitting [RRMS] and 51 secondary progressive [SPMS]) over 6 years on 3-dimensional, T1-weighted, magnetization-prepared rapid-acquisition gradient echo images. Expanded Disability Status Scale (EDSS) score and relapses were recorded at every follow-up.ResultsPatients with SPMS had lower baseline SCV (p < 0.01) but no accelerated SCV loss compared to those with RRMS. Clinical relapses were found to predict SCV loss over time (p < 0.05) in RRMS. Furthermore, SCV loss, but not total brain volume and T2 lesion volume, was a strong predictor of EDSS score worsening over time (p < 0.05). The mean annual rate of SCV loss was the strongest MRI predictor for the mean annual EDSS score change of both RRMS and SPMS separately, while correlating stronger in SPMS. Every 1% increase of the annual SCV loss rate was associated with an extra 28% risk increase of disease progression in the following year in both groups.ConclusionSCV loss over time relates to the number of clinical relapses in RRMS, but overall does not differ between RRMS and SPMS. SCV proved to be a strong predictor of physical disability and disease progression, indicating that SCV may be a suitable marker for monitoring disease activity and severity.

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Schmidt, Meic H., Paul Klimo, and Frank D. Vrionis. "Metastatic Spinal Cord Compression." Journal of the National Comprehensive Cancer Network 3, no. 5 (September 2005): 711–19. http://dx.doi.org/10.6004/jnccn.2005.0041.

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Approximately 70% of cancer patients have metastatic disease at death. The spine is involved in up to 40% of those patients. Spinal cord compression may develop in 5% to 10% of cancer patients and up to 40% of patients with preexisting nonspinal bone metastasis (>25,000 cases/y). Given the increasing survival times of patients with cancer, greater numbers of patients are likely to develop this complication. The role of surgery in the management of metastatic spinal cord compression is expanding. The management of metastatic spine disease can consist of a combination of surgery, radiation treatment, and chemotherapy. Treatment modalities are not mutually exclusive and must be individualized for patients evaluated in a multidisciplinary setting.

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Ochs, Günter, Claus Naumann, Milan Dimitrijevic, and Marc Sindou. "Intrathecal Baclofen Therapy for Spinal Origin Spasticity: Spinal Cord Injury, Spinal Cord Disease, and Multiple Sclerosis." Neuromudulation: Technology at the Neural Interface 2, no. 2 (April 6, 2002): 108–19. http://dx.doi.org/10.1046/j.1525-1403.1999.00108.x.

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da Costa, Leodante, Amir R. Dehdashti, and Karel G. terBrugg E. "Spinal cord vascular shunts: spinal cord vascular malformations and dural arteriovenous fistulas." Neurosurgical Focus 26, no. 1 (January 2009): E6. http://dx.doi.org/10.3171/foc.2009.26.1.e6.

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Object Spinal cord vascular malformations are rare, fascinating lesions. In this paper, the authors' goal was to demonstrate how these lesions, more specifically spinal cord arteriovenous malformations and dural arteriovenous fistulas, are assessed, classified, and managed at their institution. They also highlight some aspects of classification and management that may be different from the views of others. Methods The authors reviewed the 20-year experience at the senior author's institution regarding the management of spinal cord vascular malformations. They discuss the management, surgical and endovascular treatment results, and the classification that resulted from the combined experience of 3 major reference centers. Results The accumulated knowledge on embryological and pathophysiological aspects in such a rare disease resulted in a more global, patient-oriented (and not radiologically oriented) approach to spinal cord shunts. Conclusions The multiple classifications proposed for spinal cord vascular malformations reflect the continuous advancement of the authors' understanding. They adopt a classification based on new physiological and genetic data that treats these lesions as expressions of more complex disease processes and not simply a morphological target, with direct impact on therapeutic options.

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Negrin, Arianna, Scott Schatzberg, and Simon R. Platt. "The Paralyzed Cat." Journal of Feline Medicine and Surgery 11, no. 5 (May 2009): 361–72. http://dx.doi.org/10.1016/j.jfms.2009.03.004.

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Practical relevance Although gait disturbance is one of the most common neurological presentations in feline medicine, the clinical approach to the paralyzed cat can be challenging. After excluding orthopedic and cardiovascular diseases that may mimic a neurological condition, the clinician has to address a long list of different diseases that may affect the spinal cord and produce paresis. Clinical challenges In many cases a definitive cause of spinal weakness in cats is difficult to prove. Even when treatable diseases are identified, the prognosis is very much dependent on the severity of the clinical signs and their chronicity. This review sets out to describe the specific approach, diagnosis and management of cats with spinal cord disease and to outline the most common diseases responsible. Patient group Patients of either gender and all ages and breeds can be affected by spinal cord disease. Evidence base Many diseases affecting the spinal cord of cats, which include fibrocartilaginous embolic myelopathy, intervertebral disc disease, exogenous spinal cord trauma, spinal cord lymphosarcoma and feline infectious peritonitis, are well described in the literature. Many of these descriptions, however, have been based on case reports or series. While there have been several retrospective studies that describe the characteristics and incidence of these diseases in cats, there are no long term treatment trials or outcome studies to assist with prognostic determinations.

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Hong, Michael K. Y., Matthew K. H. Hong, Wei-Ren Pan, David Wallace, Mark W. Ashton, and G. Ian Taylor. "The angiosome territories of the spinal cord: exploring the issue of preoperative spinal angiography." Journal of Neurosurgery: Spine 8, no. 4 (April 2008): 352–64. http://dx.doi.org/10.3171/spi/2008/8/4/352.

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Object The angiosome concept has been the subject of extensive research by the senior author (G.I.T.), but its specific applicability to the spinal cord was hitherto unknown. The aim of this study was to see if the spinal cord vasculature followed the angiosome concept and to review the usefulness of preoperative spinal angiography in surgery for spinal disorders. Spinal cord infarction and permanent paraplegia may result from inadvertent interruption of the artery of Adamkiewicz. Spinal angiography, which may enable avoidance of this catastrophic complication, is still not commonly used. Methods Two fresh cadavers were injected with a gelatin–lead oxide mixture for detailed comparative study of spinal cord vasculature. One cadaver had insignificant vascular disease, whereas the other had extensive aortic atherosclerosis, presenting a unique opportunity for study. After removal from each cadaver, radiographs of the spinal cords were obtained, then photographed, and the vascular territories of the cords were defined. Results Four angiosome territories were defined: vertebral, subclavian, posterior intercostal, and lumbar. These vascular territories were joined longitudinally by true anastomotic channels along the anterior and posterior spinal cord. Anastomosis between the anterior and posterior vasculature was poor in the thoracolumbar region. The anterior cord relied on fewer feeder arteries than the posterior, and the anterior thoracolumbar cord depended on the artery of Adamkiewicz for its supply. In chronic aortic disease with intercostal artery occlusion at multiple levels, a rich collateral circulation supporting the spinal cord was found. Conclusions The arterial supply of the spinal cord follows the angiosome concept. The atherosclerotic specimen supports the suggestion that the blood supply is able to adapt to gradual vascular occlusion through development of a collateral circulation. Nevertheless, the spinal cord is susceptible to ischemia when faced with acute vascular occlusion. This includes inadvertent interruption of the artery of Adamkiewicz. The authors recommend the use of preoperative spinal angiography to prevent possible paraplegia in removal of thoracolumbar spinal tumors.

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Kou, Jiange, Maolin Cai, Fei Xie, Yixuan Wang, Na Wang, and Meng Xu. "Complex Electrical Stimulation Systems in Motor Function Rehabilitation after Spinal Cord Injury." Complexity 2021 (October 25, 2021): 1–16. http://dx.doi.org/10.1155/2021/2214762.

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Spinal cord injury (SCI) is an existing incurable disease that brings great pain and life obstacles to patients. Spinal cord electrical stimulation is an effective means to alleviate spinal cord injury. However, its complicated mechanism of action is still unclear. This article aims to summarize several different spinal cord electrical stimulation methods, analyze the stimulation effect, and briefly describe the current understanding of its origin and mechanism of action. In recent years, several application cases of the electrical stimulation system of stimulation methods have confirmed its positive effects in spinal cord injury diseases and provided new perspectives for the improvement of spinal cord injury. Finally, the possible development direction and corresponding challenges of spinal cord electrical stimulation in the future are proposed.

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Zhu, Ping, Jia-xin Li, Masayuki Fujino, Jian Zhuang, and Xiao-Kang Li. "Development and Treatments of Inflammatory Cells and Cytokines in Spinal Cord Ischemia-Reperfusion Injury." Mediators of Inflammation 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/701970.

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During aortic surgery, interruption of spinal cord blood flow might cause spinal cord ischemia-reperfusion injury (IRI). The incidence of spinal cord IRI after aortic surgery is up to 28%, and patients with spinal cord IRI might suffer from postoperative paraplegia or paraparesis. Spinal cord IRI includes two phases. The immediate spinal cord injury is related to acute ischemia. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury. Inflammation is a subsequent event of spinal cord ischemia and possibly a major contributor to spinal cord IRI. However, the development of inflammatory mediators is incompletely demonstrated. And treatments available for inflammation in spinal cord IRI are insufficient. Improved understanding about spinal cord IRI and the development of inflammatory cells and cytokines in this process will provide novel therapeutic strategies for spinal cord IRI. Inflammatory cytokines (e.g., TNF-αand IL-1) may play an important role in spinal cord IRI. For treatment of several intractable autoimmune diseases (e.g., rheumatoid arthritis), where inflammatory cytokines are involved in disease progression, anti-inflammatory cytokine antagonist is now available. Hence, there is great potential of anti-inflammatory cytokine antagonist for therapeutic use of spinal cord IRI. We here review the mediators and several possibilities of treatment in spinal cord IRI.

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Arjun and Kanchana V. "Spinal cord segmentation and classification of degenerative disease." International Journal of Research in Pharmaceutical Sciences 10, no. 3 (July 25, 2019): 2426–32. http://dx.doi.org/10.26452/ijrps.v10i3.1490.

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spinal cord plays an important role in human life. In our work, we are using digital image processing technique, the interior part of the human body can be analyzed using MRI, CT and X-RAY etc. Medical image processing technique is extensively used in medical field. In here we are using MRI image to perform our work In our proposed work, we are finding degenerative disease from spinal cord image. In our work first, we are preprocessing the MRI image and locate the degenerative part of the spinal cord, finding the degenerative part using various segmentation approach after that classifying degenerative disease or normal spinal cord using various classification algorithm. For segmentation, we are using an efficient semantic segmentation approach

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Lewis, Donald W., Roger J. Packer, Beverly Raney, Ihor W. Rak, Jean Belasco, and Beverly Lange. "Incidence, Presentation, and Outcome of Spinal Cord Disease in Children With Systemic Cancer." Pediatrics 78, no. 3 (September 1, 1986): 438–43. http://dx.doi.org/10.1542/peds.78.3.438.

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During a 40-month period, in 24 of 643 (4%) newly diagnosed patients with systemic cancer younger than 18 years of age (range: 3 months to 17 years) spinal cord disease developed. Patients with spinal cord disease included 21 children with metastatic spinal cord compression, two with treatment-related transverse myelopathies, and one with an anterior spinal artery stroke. Spinal cord disease occurred in 13 of 102 children (12%) with sarcomas, six of 82 (7%) with neuroblastomas, and four of 94 (4%) with lymphomas. Spinal cord compression occurred as the presenting sign of malignancy in six children (four with sarcomas and two with lymphomas). In the remaining 15 patients, cord compression occurred a median of 13 months after initial diagnosis, and in four patients it occurred at the time of first relapse. Symptoms of metastatic cord compression included back pain in 17 patients (80%), weakness in 14 (67%), sphincter dysfunction in 12 (57%), and sensory abnormalities in three (14%). Findings on plain radiographs of the spine were abnormal in only seven of 20 patients with cord compression, and myelography was needed to differentiate compression from other causes of spinal cord disease. Treatment included high-dose corticosteroids followed by operation (seven patients) or radiotherapy (14 patients). After treatment, nine of 15 nonambulatory patients became ambulatory, and five of 10 incontinent patients regained sphincter control. None of the patients with nonmetastatic spinal cord disease had a satisfactory outcome. Incorrect and delayed diagnosis was frequent in children with spinal cord disease (median time from onset of symptoms to diagnosis, 2 weeks) and 12 children were paraplegic and ten had loss of sphincter control at diagnosis. Spinal cord disease is a relatively common neurologic emergency in children with cancer, especially in those with sarcoma, and requires immediate investigation and intervention.

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Sotome, Akihito, Ken Kadoya, Yuki Suzuki, and Norimasa Iwasaki. "Spinal Canal and Spinal Cord in Rat Continue to Grow Even after Sexual Maturation: Anatomical Study and Molecular Proposition." International Journal of Molecular Sciences 23, no. 24 (December 16, 2022): 16076. http://dx.doi.org/10.3390/ijms232416076.

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Although rodents have been widely used for experimental models of spinal cord diseases, the details of the growth curves of their spinal canal and spinal cord, as well as the molecular mechanism of the growth of adult rat spinal cords remain unavailable. They are particularly important when conducting the experiments of cervical spondylotic myelopathy (CSM), since the disease condition depends on the size of the spinal canal and the spinal cord. Thus, the purposes of the present study were to obtain accurate growth curves for the spinal canal and spinal cord in rats; to define the appropriate age in weeks for their use as a CSM model; and to propose a molecular mechanism of the growth of the adult spinal cord in rats. CT myelography was performed on Lewis rats from 4 weeks to 40 weeks of age. The vertical growth of the spinal canal at C5 reached a plateau after 20 and 12 weeks, and at T8 after 20 and 16 weeks, in males and females, respectively. The vertical growth of the C5 and T8 spinal cord reached a plateau after 24 weeks in both sexes. The vertical space available for the cord (SAC) of C5 and T8 did not significantly change after 8 weeks in either sex. Western blot analyses showed that VEGFA, FGF2, and BDNF were highly expressed in the cervical spinal cords of 4-week-old rats, and that the expression of these growth factors declined as rats grew. These findings indicate that the spinal canal and the spinal cord in rats continue to grow even after sexual maturation and that rats need to be at least 8 weeks of age for use in experimental models of CSM. The present study, in conjunction with recent evidence, proposes the hypothetical model that the growth of rat spinal cord after the postnatal period is mediated at least in part by differentiation of neural progenitor cells and that their differentiation potency is maintained by VEGFA, FGF2, and BDNF.

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Lee, Dae Won, and Yoon Hee Choi. "Spinal cord infarction mimicking ischemic heart disease." Clinical and Experimental Emergency Medicine 4, no. 2 (June 30, 2017): 109–12. http://dx.doi.org/10.15441/ceem.16.121.

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Broseta, Jaime, José Barberá, J. A. de Vera, Juan Luis Barcia-Salorio, Guillermo Garcia-March, José González-Darder, Francisco Rovaina, and Vicente Joanes. "Spinal cord stimulation in peripheral arterial disease." Journal of Neurosurgery 64, no. 1 (January 1986): 71–80. http://dx.doi.org/10.3171/jns.1986.64.1.0071.

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✓ Percutaneous epidural Stimulation of the low thoracic spinal cord was carried out in 41 patients with pain from peripheral arterial disease of the lower limbs. Results are reported relating to pain, claudication distance, peripheral blood flow, and trophic lesion changes. Following a trial period of stimulation, 37 patients had stimulators permanently implanted. After a mean poststimulation follow-up period of 25 months, substantial pain relief (75% to 100%) was obtained in 29 cases; claudication distance significantly increased in 15 cases; Doppler ultrasound recordings of lower-limb distal arteries showed a tendency toward normalization of pulse-wave morphology, with increase of amplitude in 12 of the 23 patients studied; a rise in skin temperature was also detected by thermography. Distal arterial blood pressure remained unchanged with stimulation. Ischemic cutaneous trophic lesions of less than 3 sq cm healed, but gangrenous conditions were not benefited. A placebo effect or the natural history of the disease can be excluded as the reason for these improvements. It is concluded that spinal cord stimulation is a valid alternative treatment for moderate peripheral arterial disorders when direct arterial surgery is not possible or has been unsuccessful.

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Dran, Grégory, David Rasendrarijao, Fanny Vandenbos, and Philippe Paquis. "ROSAI-DORFMAN DISEASE CAUSING SPINAL CORD COMPRESSION." Neurosurgery 62, no. 4 (April 1, 2008): E977—E978. http://dx.doi.org/10.1227/01.neu.0000318189.56277.b8.

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Abstract OBJECTIVE Rosai-Dorfman disease is a rare idiopathic, histiocytic, proliferative disease characterized by massive, painless cervical lymphadenopathy. Extranodal involvement is rare and central nervous system involvement is unusual. We present a patient with Rosai-Dorfman disease with spinal cord compression. Very few cases have been reported in the literature. CLINICAL PRESENTATION A 17-year-old man presented with a 1-month history of progressive fatigue of the legs. His medical history was significant for Rosai-Dorfman disease diagnosed 7 months earlier. Clinical examination was consistent with a pyramidal syndrome and proprioceptive disturbances on his lower limbs without sensory level. A magnetic resonance imaging scan revealed an intradural extramedullary space-occupying lesion at the T1-T4 level with dural insertion and spinal cord compression. INTERVENTION A T1–T4 laminotomy was performed. Upon opening the dura, a reddish-gray mass was encountered, which encased the dorsal and lateral arachnoidal membrane. The lesion was relatively well circumscribed and was easily dissected from the underlying arachnoid. Pathological examination of the compressive soft tissue was consistent with Rosai-Dorfman disease. Postoperatively, the patient showed substantial improvement in neurological function. He was followed for 18 months with no complaints and no recurrence. CONCLUSION Neurosurgeons should consider this rare etiology of spinal cord compression. They must be aware that this lesion can occur in front of an intraspinal lesion, mimic meningiomas, occur in young people, and can potentially be associated with other locations of disease, including intracranial lesions. Surgery is the treatment of choice.

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Fujikawa, T., and K. Takayama. "Spinal cord abscess and inflammatory bowel disease." QJM 108, no. 3 (September 3, 2014): 253–54. http://dx.doi.org/10.1093/qjmed/hcu181.

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Lelli, S., M. Panizza, and M. Hallett. "Spinal cord inhibitory mechanisms in Parkinson's disease." Neurology 41, no. 4 (April 1, 1991): 553. http://dx.doi.org/10.1212/wnl.41.4.553.

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Goldblatt, J., P. Keet, and D. Dall. "Spinal cord decompression for Gaucher??s disease." Neurosurgery 21, no. 2 (August 1987): 227???30. http://dx.doi.org/10.1097/00006123-198708000-00017.

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Pego-Reigosa, Robustiano, Francisco Brañas-Fernández, Francisco Martínez-Vázquez, María José Rivas-Bande, Luís Sanjuanbenito, Mercedes García-Villanueva, and José Antonio Cortés-Laíño. "Erdheim-Chester Disease with Spinal Cord Manifestations." European Neurology 43, no. 4 (2000): 242–44. http://dx.doi.org/10.1159/000008166.

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Su, Ta-Wei, Tzu-Yi Chou, Herng-Jeng Jou, Pei-Yu Yang, Cheng-Li Lin, Fung-Chang Sung, Chung-Y. Hsu, and Chia-Hung Kao. "Peripheral Arterial Disease and Spinal Cord Injury." Medicine 94, no. 41 (October 2015): e1655. http://dx.doi.org/10.1097/md.0000000000001655.

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Delp, Sharon M., and Lisa A. Ruth-Sahd. "The Disease Process of Spinal Cord Injuries." Dimensions of Critical Care Nursing 24, no. 2 (March 2005): 57–63. http://dx.doi.org/10.1097/00003465-200503000-00003.

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Mossman, S., R. Kapoor, and C. J. Fowler. "Spontaneous ejaculation secondary to spinal cord disease." Journal of Neurology, Neurosurgery & Psychiatry 57, no. 4 (April 1, 1994): 505–6. http://dx.doi.org/10.1136/jnnp.57.4.505.

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Sipski, Marca L., Steven Hendler, and Joel A. DeLisa. "Rehabilitation of Patients with Spinal Cord Disease." Neurologic Clinics 9, no. 3 (August 1991): 705–25. http://dx.doi.org/10.1016/s0733-8619(18)30275-5.

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Abdel-Azim, Mohamed, Maryrose Sullivan, and Subbarao V. Yalla. "Disorders of Bladder Function Spinal Cord Disease." Neurologic Clinics 9, no. 3 (August 1991): 727–40. http://dx.doi.org/10.1016/s0733-8619(18)30276-7.

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Hammack, Julie E. "Spinal Cord Disease in Patients With Cancer." CONTINUUM: Lifelong Learning in Neurology 18 (April 2012): 312–27. http://dx.doi.org/10.1212/01.con.0000413660.58045.ae.

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Watson, Paul. "Metastatic spinal cord compression with oligometastatic disease." Oncology Times 4, no. 3 (March 2007): 11–13. http://dx.doi.org/10.1097/01434893-200703000-00012.

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Augustinsson, L. "SPINAL CORD STIMULATION IN PERIPHERAL VASCULAR DISEASE." European Journal of Pain 3, no. 4 (December 1999): 397–99. http://dx.doi.org/10.1016/s1090-3801(99)90027-7.

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Kressler, Jochen, Rachel E. Cowan, Gregory E. Bigford, and Mark S. Nash. "Reducing Cardiometabolic Disease in Spinal Cord Injury." Physical Medicine and Rehabilitation Clinics of North America 25, no. 3 (August 2014): 573–604. http://dx.doi.org/10.1016/j.pmr.2014.04.006.

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Gupta, Vivek. "Positron Emission Tomography in Spinal Cord Disease." Mayo Clinic Proceedings 88, no. 11 (November 2013): 1188–90. http://dx.doi.org/10.1016/j.mayocp.2013.09.004.

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Divers, Thomas J. "Acquired spinal cord and peripheral nerve disease." Veterinary Clinics of North America: Food Animal Practice 20, no. 2 (July 2004): 231–42. http://dx.doi.org/10.1016/j.cvfa.2004.02.008.

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Goodman, Michael L., and Dachling Pang. "Spinal Cord Injury in I-Cell Disease." Pediatric Neurosurgery 14, no. 6 (1988): 315–18. http://dx.doi.org/10.1159/000120411.

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Done, J. T., J. Woolley, V. V. Barnard, D. H. Upcott, C. N. Hebert, and S. Terlecki. "Border disease of sheep: Spinal cord morphometry." Journal of Comparative Pathology 95, no. 3 (July 1985): 325–33. http://dx.doi.org/10.1016/0021-9975(85)90036-2.

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Del Tredici, Kelly, and Heiko Braak. "Spinal cord lesions in sporadic Parkinson’s disease." Acta Neuropathologica 124, no. 5 (August 29, 2012): 643–64. http://dx.doi.org/10.1007/s00401-012-1028-y.

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Journal articles on the topic 'Spinal cord disease'

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