British Journal of Radiology (2006) 79, e123-e125
© 2006 British Institute of Radiology
doi: 10.1259/bjr/27982692
A case of syringomyelia associated with cervical spondylosis
D J A Butteriss, FRCR
and
D Birchall, FRCR
Department of Neuroradiology, Newcastle General Hospital, Westgate Road, Newcastle-upon-Tyne, Tyne and Wear NE1 1SA, UK
Correspondence: Dr Daniel Birchall
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Abstract
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Cervical spondylosis is an extremely common condition causing spinal cord compression, and yet it very rarely causes secondary syrinx formation. We report a case of cervical spondylosis with associated syringomyelia and review the possible pathogenesis of this condition.
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Case history
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A 70-year-old man presented to the neurology outpatients complaining of neck pain and weakness in all four limbs, progressing over several months. There was no other significant past history. On examination there was a spastic paraparesis and exaggerated reflexes in the upper limbs. A presumptive clinical diagnosis of cervical spondylotic myelopathy was made. The patient was subsequently referred for MRI. Sagittal and axial T1 and T2 weighted sequences through the cervical and thoracic spine were performed, with additional post-contrast sequences. This demonstrated severe degenerative changes at C5/6 with a large right paracentral disc-osteophyte complex flattening the cord and significantly narrowing the right neural exit foramen (
Figures 1 and 2). Less marked thecal compression with a degree of bilateral exit foraminal narrowing was present at C6/7. An unexpected cord syrinx was noted extending from C6/7 inferiorly to T6 (Figures 3 and 4).
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Figure 1. SagittalT2 weighted image through the cervical spine demonstrating spondylotic changes at C5/6 and C6/7 with cord compression and caudal syrinx formation.
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Figure 2. AxialT2 weighted image at C5/6 level demonstrating right-sided cord compression by disc-osteophyte complex.
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Figure 3. SagittalT2 weighted image through the thoracic spine demonstrating mild scoliosis and wide syrinx extending to the level of T6.
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The craniocervical junction was normal, with no evidence of Chiari malformation. No cord mass lesion was demonstrated, and no other potential cause of syrinx was identified.
Detailed questioning revealed no evidence to suggest previous spinal trauma or infection. No symptoms consistent with spinal ischaemia or infarct were elicited.
The patient declined decompressive surgery.
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Discussion
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Syringomyelia, characterized by fluid-filled cavities extending longitudinally along the cord, is rarely a primary disease process, and usually occurs secondary to one of a number of disease processes. It is most commonly associated with extrinsic compressive lesions at the craniovertebral junctions, such as in the Chiari malformation. Other causes include spinal arachnoiditis and intramedullary spinal tumours. Acute traumatic cervical spinal stenosis due to fracture or acute severe disc prolapse may result in secondary syrinx formation; in this case, the mechanism is thought to be due to liquifactive necrosis of the injured cord and the syrinx is often initially localized to the site of the injury. Subsequent elongation of the syrinx may occur due to altered hydrostatic effects, such as a "one-way valve" process. Spinal spondylosis is an extremely common condition that has only rarely been described as a cause of syringomyelia [1–4].
The aetiology of syringomyelia in association with cervical spondylosis is not completely understood. The most recent theory suggests that subarachnoid obstruction, of whichever cause, predisposes to formation of transient increases in cerebrospinal fluid (CSF) pressure above the block, compared with below. Transmural hydrostatic effects may result in the collapse of vessels within the subarachnoid space above the block, and their dilatation below it. This may result in a combination of mechanical stress on the cord parenchyma and disruption of the blood–brain barrier, which in concert with raised intravascular pressure results in ultrafiltration of crystalloids and accumulation of fluid [5]. The fluid may dissect along planes of weakness within the cord resulting in the pathological appearance of a syrinx. It has been postulated that the development of high fluid pressure and syrinx formation within the cord may act to counteract the local effect of the primary compressive lesion and as such may be a protective phenomenon [6].
What is not clear is why syringes develop so rarely in cervical spondylosis, when cord compression and myelopathy are relatively common findings. It may simply be that the degree and/or duration of CSF obstruction are not usually great enough in cases of spondylosis to engender a syrinx. Acute severe compression is usually treated emergently, and the intermittent, milder compression usually seen in degenerate cervical spines may not result in the long-term abnormal hydrostatic pressures found in congenital conditions or neoplasia. The absence of any other predisposing cause in our and other cases, as well as cases demonstrating collapse of the syrinx and improvement of related symptoms after decompressive surgery [1, 2], suggest that there is a genuine causative link between spondylosis and syringomyelia, rather than a simple coincidence. Increasing MRI of spinal degenerative disease at earlier stages may help to elucidate the processes and pathways involved in syrinx formation. Nonetheless, in current practice the concurrence of cervical spondylosis and syrinx should warrant a detailed medical history and examination of imaging findings to exclude another cause for syrinx formation; in particular, post-gadolinium T1 weighted sequences should be considered to help exclude a neoplastic cause. In cases of syrinx due to spondylosis, as with other cases of secondary syrinx formation, treatment should be directed toward relieving the compressive lesion, rather than primary drainage of the syrinx.
Received for publication June 21, 2005.
Revision received September 14, 2005.
Accepted for publication November 25, 2005.
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References
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Abstract
Case history
