无波特的髓性科克病:在几内亚科纳克里大学医院中心观察到13例。

Iranian Journal of Neurology Pub Date : 2018-10-07
Fode Abass Cisse, Foksouna Sakadi, Nana Rahamatou Aminou Tassiou, Amadou Talibe Balde, Arcel Steven Nitcheu Woga, Aissatou Kenda Bah, Souleymane Djigue Barry, Ibrahima Sory Souare, Mohamed Lamine Toure, Amara Cisse
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引用次数: 0

摘要

背景:尽管磁共振成像(MRI)数据的可用性越来越高,生物探测平台也越来越完善,但在传染性、寄生性和全身性脊髓病大量存在的热带环境中,没有波特病的髓质结核(TB)的诊断确定性很难确立。方法:回顾性分析2008年至2016年在几内亚科纳克里大学医院中心神经内科和神经外科治疗非压缩性和压缩性脊髓病的186例患者的资料。13例(6.9%)患者有结核感染的生物学证据。结果:11例(84.6%)患者在出现神经系统症状前有感染性临床表现。神经学症状总结为:11例患者(84.6%)存在渐进发展的敏感-运动符号,伴括约肌疾病(100%);4例患者(30.8%)从一开始就有伴病变和病变下综合征的髓质压迫症状。9例非压缩性脊髓病患者髓质MRI显示广泛髓内高信号,其中4例病变出现T1高信号,T2等信号局限。腰椎穿刺(LP)显示淋巴细胞增多,低血糖(0.3 ~ 0.5 g/l),白细胞增多。结论:本研究揭示了压缩性和非压缩性脊髓病的典型临床、生物学、神经放射学和进化特征。这些结果对于TB脊髓病的治疗和进化讨论对于良好的管理是重要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Medullar Kock without Pott: 13 cases observed at the university hospital center of Conakry, Guinea.

Medullar Kock without Pott: 13 cases observed at the university hospital center of Conakry, Guinea.

Background: The diagnostic certainty of medullar tuberculosis (TB) without Pott disease is difficult to establish in a tropical environment with the large group of infectious, parasitic, and systemic myelopathies, despite the increasing availability of magnetic resonance imaging (MRI) data and improvement of biological exploration platforms. Methods: We retrospectively analyzed the files of 186 patients hospitalized in the Department of Neurology and Neurosurgery of the University Hospital Center of Conakry, Guinea, between 2008 and 2016 for the management of non-compressive and compressive myelopathy. Biological evidence of TB infection was demonstrated for 13 (6.9%) patients. Results: Infectious clinical picture prior to the development of neurological signs was reported in 11 patients (84.6%). The neurological signs were summed up by the existence of a sensitivo-motor semiology of progressive evolution (100% of cases) with sphincter disorders in 11 patients (84.6%) and a medullary compression symptomatology with a lesion and under lesion syndrome from the outset in 4 patients (30.8%). Medullary MRI revealed an extensive intramedullary hypersignal in 9 patients with non-compressive myelopathy and in 4 cases, the lesions appeared in T1 hypersignal and T2 isosignal were localized. Lumbar puncture (LP) revealed lymphocytic pleocytosis, hypoglucorrhage (0.3 to 0.5 g/l), and leukocytosis. Conclusion: This study reveals a classic clinical, biological, neuroradiological, and evolutionary profile of compressive and non-compressive myelopathies. These results are important for the therapeutic and evolutionary discussion of TB myelopathies for good management.

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Iranian Journal of Neurology
Iranian Journal of Neurology CLINICAL NEUROLOGY-
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