Gardner W J, McMurray F G
Surg Neurol. 1976 Oct;6(4):251-6.
Encroachment by man's overlarge forebrain is responsible for the anatomic substrate of syringomyelia, i.e. a hindbrain hernia developing in fetal life with persisting hydromyelia. Communication between the syrinx and 4th ventricle is readily disclosed at operation, but because of postmortem shrinkage, almost never at autopsy. Syringomyelia developing in 16 of 864 post-traumatic paraplegics has been classified non-communicating. However, the syrinx, its fluid, and the ultimate clinical picture are the same as in the non-traumatic, and surgical exposure has disclosed the communication. The symptoms develop because the traumatic subarachnoid block exaggerates the causative intracranial fluid pulse waves by eliminating the dampling effect of the yielding dural sac below. A non-traumatic spinal block also may result in syringomyelia.
人类过大的前脑侵犯是脊髓空洞症解剖学基础的原因,即胎儿期发生的后脑疝伴持续性脊髓积水。手术中很容易发现脊髓空洞与第四脑室之间的连通,但由于死后组织收缩,尸检时几乎从未发现。864例创伤后截瘫患者中有16例发生的脊髓空洞症被归类为非交通性。然而,脊髓空洞、其内含液体以及最终的临床表现与非创伤性脊髓空洞症相同,手术暴露已发现了连通情况。症状的出现是因为创伤性蛛网膜下腔阻塞消除了下方可顺应性硬脊膜囊的阻尼作用,从而夸大了导致脊髓空洞症的颅内液体脉搏波。非创伤性脊髓阻滞也可能导致脊髓空洞症。