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AJNR Am J Neuroradiol 20:7±20, January 1999 The ``Presyrinx'' State: A Reversible Myelopathic Condition That May Precede Syringomyelia Nancy J. Fischbein, William P. Dillon, Charles Cobbs, and Philip R. Weinstein BACKGROUND AND PURPOSE: Alteration of CSF ¯ow has been proposed to be an important mechanism leading to the development of syringomyelia. We hypothesize that a ``presyrinx'' con- dition attributable to a potentially reversible alteration in normal CSF ¯ow 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 ¯ow, and no evidence of intramedullary tumor or a spinal vascular event underwent MR imaging before and after intervention that alleviated obstruction to CSF ¯ow. 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. Syringomyelia occurs in a number of clinical set- ated with the development of different types of sy- tings, most commonly after trauma (1±3) or in as- ringomyelia (18, 26) and most likely play a role in sociation with a Chiari malformation (4±7). Other determining the location of a syrinx remote from a causes include infectious or in¯ammatory arach- focus of CSF obstruction, such as is commonly noiditis (7±11), tumors of the spine and spinal cord seen in the Chiari I malformation. The reversibility (7), posterior fossa tumors (12), and cervical spon- of syringomyelia after restoration of CSF pathways dylosis (13). Syrinxes typically appear as well-de- has been well documented in patients undergoing ®ned discrete cavities containing ¯uid that is isoin- posterior fossa decompression for Chiari malfor- tense with CSF on all sequences (14, 15). The mations, removal of extradural masses, and lysis of pathophysiology of syringomyelia is controversial, adhesions (9, 12, 27). but experimental models (16±18) and clinical stud- We have identi®ed ®ve myelopathic patients ies (19) have implicated alterations in CSF ¯ow as with no history of spine trauma who had underly- a signi®cant factor in the development and pro- ing conditions associated with alterations of CSF gression of certain types of syringomyelia. The hy- ¯ow. These patients had enlargement and T2 pro- pothesis that CSF normally ¯ows along perivas- longation of the spinal cord, without frank cavita- cular spaces within the parenchyma of the spinal tion, on MR imaging studies that improved or re- cord to the central canal is supported by experi- versed after restoration of CSF ¯ow pathways. We mental studies (20±25). Variations in patency of the hypothesized on the basis of historical, imaging, central canal of the spinal cord have been associ- and surgical ®ndings that obstruction to normal CSF ¯ow pathways resulted in the cord enlarge- ment and MR signal abnormalities that reversed af- Received March 10, 1998; accepted after revision August 26. ter restoration of normal CSF pathways. We also From the Departments of Radiology (N.J.F., W.P.D.) and hypothesized that variation in patency of the central Neurosurgery (C.C., P.R.W.), University of California, San Francisco. canal of the spinal cord plays a role in the genesis Address reprint requests to Nancy J. Fischbein, MD, De- of this ``presyrinx'' state. partment of Radiology, Box 0628, University of California, San Francisco, 505 Parnassus Ave, San Francisco, CA 94143. Methods Over a 2-year period, ®ve patients who met the following q American Society of Neuroradiology criteria were identi®ed prospectively: clinical evidence of my- 7 8 FISCHBEIN AJNR: 20, January 1999 Summary of Patient Data Patient Figure No. Age (y)/Sex History Clinical Condition Pre-op Previous Surgery 1 1 2/M Chiari I malformation Severe headaches, progressive Limited decompression (suboc- clumsiness in limb move- cipital craniectomy) for ments over the course of 1 y Chiari I malformation 2 2 69/F Polymyalgia rheumatica, previ- Progressive quadriparesis, pro- Decompression of epidural ab- ous epidural abscess associ- gressive loss of sensation scess via C6 laminectomy ated with osteomyelitis of and motor control in hands 18 mo earlier the cervical spine 3 4 41/M Remote h/o head trauma; basi- Progressive neck pain and Posterior fossa decompression lar arachnoid adhesions; h/o spastic quadriparesis VP shunt for hydrocephalus hydrocephalus 4 3 40/F Grade III SAH caused by an- Neck pain and quadriparesis Coil embolization of aneu- eurysm, s/p GDC coil em- rysm, external ventricular bolization; course c/b S. epi- drainage of CSF dermidis meningitis 5 NS 77/F Severe cervical spondylosten- Progressive weakness in both None osis and mild basilar im- arms, R . L, and hand pression numbness; spasticity and in- coordination of legs; no neck pain Note.ÐFM indicates foramen magnum; SAH, subarachnoid hemorrhage; NS, not shown; VP, ventriculoperitoneal; S. epidermidis, Staphylococcus epidermidis; h/o, history of; pre-op, preoperatively; post-op, postoperatively. elopathy, no history of spinal cord trauma, enlargement of the Table. All patients underwent MR imaging of the cervical cord with parenchymal T1 and T2 prolongation but cervical spinal cord to evaluate myelopathic symp- no frank cavitation, and no evidence of intramedullary tumor or a spinal vascular event as the cause of cord signal changes. toms, although in one case (patient 1) headaches No patient had evidence of active in¯ammatory or demyelin- were the dominant clinical feature. The clinical pre- ating disease or received steroid therapy. In addition, all pa- sentations were similar to that of patients with cen- tients had obstruction to CSF ¯ow at the level of the foramen tral cystic myelopathy (7, 28), including increasing magnum or the spinal epidural or subarachnoid space as evi- loss of motor function or weakness in all patients, denced by historical and/or imaging ®ndings. Our patients in- sensory changes in two patients, increased spastic- cluded two males and three females and ranged in age from 2 to 77 years. Clinical records and imaging studies for these ity in two patients, and radicular pain in one pa- patients were reviewed. tient. The conditions that predisposed our patients All patients underwent preoperative imaging on a 1.5-T MR to alterations in CSF ¯ow dynamics and myelop- system. Imaging sequences included conventional spin-echo athy included the following: Chiari I malformation T1-weighted images (500/14 [TR/TE], 4 mm thick, 256 3 256 with severe tonsillar herniation; previous osteo- matrix) and fast spin-echo T2-weighted images (3000/105eff, myelitis complicated by epidural abscess, menin- echo train length of 8, 3 mm thick, 256 3 256 matrix) obtained in the sagittal plane in addition to axial T1-weighted images. gitis, and arachnoiditis; basilar arachnoid adhesions A proton density±weighted sequence was not obtained, since related to previous head trauma, traumatic sub- it is not part of our routine spine imaging protocol. Contrast- arachnoid hemorrhage, and posterior fossa surgery; enhanced images were obtained in three patients and included subarachnoid hemorrhage complicated by menin- sagittal and axial T1-weighted sequences. MR examinations gitis, leading to severe hydrocephalus and tonsillar were conducted on all patients after surgical intervention and included, at a minimum, sagittal T1-weighted and fast spin- herniation; and rheumatoid arthritis with severe echo T2-weighted sequences. In addition, one patient under- cervical spondylosis and spinal stenosis accompa- went CT myelography preoperatively, and one patient under- nied by basilar impression. In all ®ve cases, the went CT myelography postoperatively. Only one patient had lesion occurred in the cervical spinal cord. an MR ¯ow study performed preoperatively, using a cine Results of preoperative MR imaging revealed a phase-contrast technique (24/minimum [TR/TE], ¯ip angle of 308, 256 3 128 matrix, ¯ow compensation and peripheral gat- variable degree of enlargement of the cervical cord ing applied, velocity-encoding gradient 5 5 cm/s) to evaluate in all patients. All patients had abnormal T1 and CSF ¯ow at the foramen magnum. T2 prolongation of the cervical spinal cord signal extending over a variable distance. The T1 signal Results was not as low as CSF in any case, and the margins A summary of our patients' histories, as well as of the T1 signal abnormality were not sharply de- clinical and imaging ®ndings, is presented in the ®ned. No frank cavitation was observed in any pa- AJNR: 20, January 1999 ``PRESYRINX'' STATE 9 TABLE 1: Continued. MR Findings Pre-Op Surgical Intervention Clinical Findings Post-op MR Findings Post-op Progressive T1 and T2 prolon- Aggressive suboccipital de- Improved
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