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“脊髓空洞前”状态:一种可能先于脊髓空洞症出现的可逆性脊髓病状态。

The "presyrinx" state: a reversible myelopathic condition that may precede syringomyelia.

作者信息

Fischbein N J, Dillon W P, Cobbs C, Weinstein P R

机构信息

Department of Radiology, University of California, San Francisco 94143, USA.

出版信息

AJNR Am J Neuroradiol. 1999 Jan;20(1):7-20.

PMID:9974051
Abstract

BACKGROUND AND PURPOSE

Alteration of CSF flow has been proposed to be an important mechanism leading to the development of syringomyelia. We hypothesize that a "presyrinx" condition attributable to a potentially reversible alteration in normal CSF flow exists and that its appearance may be caused by variations in the competence of the central canal of the spinal cord.

METHODS

Five patients with clinical evidence of myelopathy, no history of spinal cord trauma, enlargement of the cervical spinal cord with T1 and T2 prolongation but no cavitation, evidence of altered or obstructed CSF flow, and no evidence of intramedullary tumor or a spinal vascular event underwent MR imaging before and after intervention that alleviated obstruction to CSF flow.

RESULTS

Preoperatively, all patients had enlarged spinal cords and parenchymal T1 and T2 prolongation without cavitation. Results of MR examinations after intervention showed resolution of cord enlargement and normalization or improvement of cord signal abnormalities. In one patient with severe arachnoid adhesions who initially improved after decompression, late evolution into syringomyelia occurred in association with continued CSF obstruction.

CONCLUSION

Nontraumatic obstruction of the CSF pathways in the spine may result in spinal cord parenchymal T2 prolongation that is reversible after restoration of patency of CSF pathways. We refer to this MR appearance as the "presyrinx" state and stress the importance of timely intervention to limit progression to syringomyelia.

摘要

背景与目的

脑脊液流动改变被认为是导致脊髓空洞症发生的重要机制。我们假设存在一种由正常脑脊液流动的潜在可逆改变引起的“脊髓空洞前”状态,并且其出现可能是由脊髓中央管功能的变化所致。

方法

5例有脊髓病临床证据、无脊髓外伤史、颈髓增粗且T1和T2信号延长但无空洞形成、有脑脊液流动改变或梗阻证据、无髓内肿瘤或脊髓血管病变证据的患者,在缓解脑脊液流动梗阻的干预前后接受了磁共振成像检查。

结果

术前,所有患者脊髓均增粗,实质T1和T2信号延长且无空洞形成。干预后的磁共振检查结果显示脊髓增粗消退,脊髓信号异常恢复正常或改善。1例有严重蛛网膜粘连的患者在减压后最初有所改善,但后期随着脑脊液持续梗阻演变为脊髓空洞症。

结论

脊柱脑脊液通路的非创伤性梗阻可能导致脊髓实质T2信号延长,在脑脊液通路恢复通畅后可逆转。我们将这种磁共振表现称为“脊髓空洞前”状态,并强调及时干预以限制进展为脊髓空洞症的重要性。

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