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


CONCLUSIONS
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.
Fischbein
N J
NJ
Department of Radiology, University of California, San Francisco 94143, USA.
Dillon
W P
WP
Cobbs
C
C
Weinstein
P R
PR
D000328:Adult; D000368:Aged; D002555:Cerebrospinal Fluid / Q000502:physiology; D002675:Child, Preschool; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology; D013595:Syringomyelia / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*