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Spine J. 2016 Nov;16(11):e751-e754. doi: 10.1016/j.spinee.2016.06.003. Epub 2016 Jun 9.

Venous hypertensive myelopathy associated with cervical spondylosis.

Author information

1
Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, 800 Howard Ave, New Haven, CT 06520, USA; Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
2
Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, 800 Howard Ave, New Haven, CT 06520, USA.
3
Department of Radiology, University of California San Diego, 200 West Arbor Dr, San Diego, CA 92103-0834, USA.
4
Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, 800 Howard Ave, New Haven, CT 06520, USA. Electronic address: james.yue@yale.edu.

Abstract

BACKGROUND CONTEXT:

Venous hypertensive myelopathy (VHM) results from spinal vascular malformations of arteriovenous shunting that increases spinal venous pressure, leading to congestive edema and neurologic dysfunction. There has been no report of VHM associated with cervical spondylotic myelopathy (CSM).

PURPOSE:

The aim of this study was to report an extremely rare case of VHM likely due to CSM.

STUDY DESIGN:

This study is a case report and review of the literature.

PATIENT SAMPLE:

The patient was a 51-year-old man with CSM exhibiting relatively rapid neurologic deterioration with an abnormal expansion of a centromedullary hyperintense lesion on T2-weighted magnetic resonance imaging (MRI) in the absence of traumatic injury.

METHODS:

Neurologic examination and radiologic imaging were taken by various means.

RESULTS:

The patient developed a cervical radiculopathy, followed by gait disturbance and motor weakness. The MRI of the cervical spine demonstrated spinal canal stenosis due to disc bulging and flavum hypertrophy at the C5/C6 and C6/C7 levels as well as hyperintense area over the C5-C7 levels on T2-weighted images. Although decompression surgery was planned, an acute inflammatory process such as transverse myelitis or demyelinating disease other than cord compression was also considered, and the patient received intravenous steroids. His walking improved for several days. However, his symptoms then became significantly worse, and he had difficulty walking. Subsequent MRI demonstrated marked progression of the T2 hyperintense lesion over the C4-T1 vertebral levels. Flow voids were also noted on the dorsal surface of the upper cervical cord on T2-weighted MRI. His lab work, medical history, and the local enhancement on contrast-enhanced MRI indicated low probability of spinal inflammatory diseases. Therefore, the decision was made to perform anterior cervical discectomy and fusion surgery on two levels. Following surgery, his symptoms improved promptly.

CONCLUSIONS:

Our case indicates that VHM could be caused by spondylotic cord compression in the absence of spinal vascular malformations. The diagnostic features for VHM are progressive deterioration of myelopathy, easing/worsening of symptoms associated with postural changes, and centromedullary hyperintensity over multiple segments and the flow voids on dorsal surface of the spinal cord on T2-weighted MRI.

KEYWORDS:

Ascending myelopathy; Diagnosis; Magnetic resonance image; Spinal inflammatory diseases; Spondylosis; Venous hypertensive myelopathy

PMID:
27293119
DOI:
10.1016/j.spinee.2016.06.003
[Indexed for MEDLINE]
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