On the Pathogenesis of Syringomyelia: A Review 1
On the Pathogenesis of Syringomyelia: A Review 1
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脊髓空洞症的发病机制：综述 1
DOI：
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发表时间：
1980
影响因子：
17.3
通讯作者：
B. Williams
中科院分区：
文献类型：
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作者：
B. Williams
对脊髓空洞症发病机制的讨论涉及考虑液体的来源以及导致液体破坏脊髓结构的力。当脑脊液 (CSF) 似乎是破坏性元素时，它通常通过从第四脑室延伸到鸣管内部的开放的中央管进入。在临床和实验情况下，可以测量压力差，该压力差吸吮后脑，特别是小脑扁桃体，产生畸形。这些压力差也可能将液体吸入注射管。在其他情况下，即使沟通似乎并不明显，后脑异常通常也存在，并且通常可以证明吸吮效应，并且其纠正伴随着临床改善。注射管内的其他液体来源包括外伤性截瘫后血肿的液化以及来自内在脊柱肿瘤的液体渗出。一旦脊髓腔内存在液体，它可能会响应蛛网膜下腔中的液体运动而向上和向下脉动，其中最活跃的液体运动是由静脉影响引起的。这种“晃动”运动可能会导致空腔在两端延伸，从而导致创伤后脊髓囊肿向上和向下延伸，有时甚至导致脊髓空洞症。脊髓缺血、静脉充血和沿着血管周围空间的液体输送都可能在维持脊髓腔或临床残疾的进展中发挥作用。
Discussion of the pathogenesis of syringomyelia involves considering the origin of the fluid and also the forces which cause that fluid to break down the structure of the cord. When cerebrospinal fluid (CSF) appears to be the destructive element, it commonly enters through a patent central canal running from the fourth ventricle to the inside of the syrinx. In both clinical and experimental situations pressure differences may be measured which suck on the hindbrain, particularly the cerebellar tonsils, producing deformities. These pressure differences may also suck fluid into the syrinx. In other cases, even when a communication does not appear to be patent, the hindbrain abnormalities are usually present and suck effect may usually be demonstrated and its correction be accompanied by clinical improvement. Other sources of fluid within a syrinx include liquefaction of haematomata after traumatic paraplegia and transudation of fluid from intrinsic spinal tumours. Once fluid is present within a cord cavity it may pulsate upwards and downwards in response to fluid movements in the subarachnoid space, the most energetic of which result from venous influences. Such movement, ‘slosh’, may cause the cavities to extend at either end giving rise to upward and downward extension from a post-traumatic cord cyst and sometimes to syringobulbia. Cord ischaemia, venous congestion and transport of fluid along perivascular spaces may all play a part in the maintainance of cord cavities or the progression of the clinical disabilities.