Spinal cord myelopathy attributed to bilateral jugular vein occlusion and impaired venous drainage....
This gal had demyelinating lesions (just like MS) on her spinal cord because her jugular veins were blocked. This is the disease model we are seeing in patients tested by Drs. Zamboni and Dake.
Ventriculoperitoneal shunt failure causing myelopathy in a
patient with bilateral jugular vein occlusion
WILLIAME. HUMPHRIES, M.P.H.,1PETERM. GROSSI, M.D.,1LINDAG. LIETHE, M.D.,2
ANDTIMOTHYM. GEORGE, M.D.3
Pediatric Neurosurgery Service, Division of Neurosurgery; 2Division of Neuroradiology, Duke University Medical Center, Durham, North Carolina; and 3Pediatric Neurosurgery, Children’s Hospital of Austin, Texas
The authors describe the case of a 36-year-old woman with bilateral internal jugular vein occlusion, hydrocephalus, and Dandy–Walker variant who presented with myelopathy that was ultimately attributed to ventriculoperitoneal (VP) shunt failure. Computed tomography (CT) angiography of the head and neck revealed epidural venous engorgement
within the cervical spine, greater that 50% narrowing of the C2–5 spinal canal, and compression of the cervical spinal cord. After successful shunt revision, postoperative CT angiography revealed decreased venous engorgement as well as decompression of the cervical spinal cord, and the patient’s myelopathy improved. This case represents a fascinat-
ing clinical presentation of VP shunt failure, highlighting the physiological importance of the external jugular pathways involved in cerebral venous drainage.
Authors of previous studies have suggested that the vertebral venous system should be adept at tolerating increased venous drainage when internal jugular venous flow is compromised, thereby raising the question as to if there were physiological consequences associated with bi-lateral IJV resection including facial cyanosis and edema.5
These complications illustrate that although the vertebral venous system can drain the cranial vault, it may not be as adept as the jugular venous system at tolerating large increases in flow. In addition, events that alter or impede distal outflow through the vertebral venous system can further compromise the ability of this system to tolerate increases in venous flow. Of interest, our patient underwent resection of a thoracic arachnoid cyst 3 years prior to presentation. Removal of this cyst may have disrupted the distal outflow of the vertebral venous network in the thoracic spine, thereby decreasing its ability to tolerate sub-
stantial increases in flow. Therefore the pathophysiology of this patient’s presentation can be attributed to a primary anatomical predisposition and a secondary acquired insult that ultimately led to spinal cord myelopathy in association with VP shunt failure.
This case illustrates a fascinating clinical presentation of VP shunt failure that highlights the physiological importance of the external jugular pathways of cerebral venous drainage.
And after correct drainage was restored...the myelopathy began to heal!!!