Published online Jun 16, 2013. doi: 10.12998/wjcc.v1.i3.111
Revised: April 11, 2013
Accepted: May 16, 2013
Published online: June 16, 2013
Processing time: 131 Days and 22.5 Hours
Spinal spondylosis is an extremely common condition that has only rarely been described as a cause of syringomyelia. We describe a case of syringomyelia associated with cervical spondylosis admitted at our division and treated by our institute. It is the case of a 66-year-old woman. At our observation she was affected by moderate-severe spastic tetraparesis. T2-weighted magnetic resonance imaging (MRI) showed an hyperintense signal within spinal cord from C3 to T1 with a more sharply defined process in the inferior cervical spinal cord. At the same level bulging discs, facets and ligamenta flava hypertrophy determined a compression towards subarachnoid space and spinal cord. Spinal cord compression was more evident in hyperextension rather than flexion. A 4-level laminectomy and subsequent posterior stabilization with intra-articular screws was executed. At 3-mo follow up there was a regression of tetraparesis but motor deficits of the lower limbs residuated. At the same follow up postoperative MRI was executed. It suggested enlargement of the syrinx. Perhaps hyperintensity within spinal cord appeared “bounded” from C3 to C7 with clearer margins. At the level of surgical decompression, subarachnoid space and spinal cord enlargement were also evident. A review of the literature was executed using PubMed database. The objective of the research was to find an etiopathological theory able to relate syringomyelia with cervical spondylosis. Only 6 articles have been found. At the origin of syringomyelia the mechanisms of compression and instability are proposed. Perhaps other studies assert the importance of subarachnoid space regard cerebrospinal fluid (CSF) dynamic. We postulate that cervical spine instability may be the cause of multiple microtrauma towards spinal cord and consequently may damage spinal cord parenchyma generating myelomalacia and consequently syrinx. Otherwise the hemorrhage within spinal cord central canal can cause an obstruction of CSF outflow, finally generating the syrinx. On the other hand in cervical spondylosis the stenotic elements can affect subarachnoid space. These elements rubbing towards spinal cord during movements of the neck can generate arachnoiditis, subarachnoid hemorrhages and arachnoid adhesions. Analyzing the literature these “complications” of cervical spondylosis are described at the origin of syringomyelia. So surgical decompression, enlarging medullary canal prevents rubbings and contacts between the bone-ligament structures of the spine towards spinal cord and subarachnoid space therefore syringomyelia. Perhaps stabilization is also necessary to prevent instability of the cervical spine at the base of central cord syndrome or syringomyelia. Finally although patients affected by central cord syndrome are usually managed conservatively we advocate, also for them, surgical treatment in cases affected by advanced state of the symptoms and MRI.
Core tip: Our study assume that central cord syndrome can result in syringomyelia. We postulate that cervical spine instability may be the cause of myelomalacia and consequently syrinx. In cervical spondylosis with related central cord syndrome or syringomyelia we underline the importance of surgical decompression and stabilization. Surgical decompression prevents “complications of cervical spondylosis” at the base of syringomyelia. Stabilization is also necessary to prevent instability of the cervical spine at the base of central cord syndrome or syringomyelia. Finally we propose the surgical treatment also for patients affected by central cord syndrome showing advanced state of the symptoms and magnetic resonance imaging.