J Neurosurg 71:938-941, 1989 Intervertebral disc embolization resulting in spinal cord infarction Case report JOHN R. W. KESTLE, B.Sc., M.D., LOTHAR RESCH, M.D., F.R.C.P.(C), CHARLES H. TATOR, M.D., PH.D., F.R.C.S.(C), AND WALTER KUCHARCZYK, M.D., F.R.C.P.(C) Department of Neuropathology and Division of Neurosurgery, Toronto Western Hospital, and Department of Radiology, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada ~," A case of spinal cord infarction resulting from embolization of fibrocartilaginous intervertebral disc material is presented. Cases from the literature are reviewed and the theories of pathogenesis are discussed. In all reported cases the diagnosis was not made until postmortem examination. KEY WORDS 9 embolization 9 nucleus pulposus 9 paraplegia 9 spinal cord infarction A CASE of spinal cord infarction as a result of embolization of intervertebral disc material is presented. Although it is rare, this entity has been reported in the pathology and neurology litera- ture. ~-4"9-~8The published cases are reviewed and the theories of pathogenesis discussed. Case Report This 43-year-old right-handed man with a 3-week history of low backache was first evaluated in the emergency department of the referring hospital. On the morning of admission the patient was awakened by a severe ache in the buttocks and posterior aspect of the thighs which did not radiate below the knees. Numbness and weakness of the feet developed over the next few hours so that the patient could not walk or stand. One month prior to admission he had suffered a flu-like illness which had resolved. There was no history of trauma or strain to the back. Examination and Hospital Course. The initial examination revealed bilateral loss of pinprick appre- ciation in a stocking distribution up to the midcalf. Vibration sensation was normal. There was complete paralysis of ankle plantar flexor and dorsiflexor mus- cles and weakness of the knee flexor, hip flexor, and hip extensor muscles. Ankle jerks were absent and the knee jerks were markedly decreased bilaterally. The ce- rebrospinal fluid (CSF) was normal except that the level of protein was elevated to 0.50 gm/liter. A computer- ized tomography (CT) scan of the spine from T-11 to the sacrum was normal. The provisional diagnosis was Guillain-Barr6 syndrome. Two days after admission there was a sudden onset of severe lumbosacral pressure-like pain, followed (in less than 30 minutes) by complete paraplegia with a sensory level at T-10. Myelography and abdominal ultrasonography were performed that day with com- pletely normal results. The CSF findings were un- changed. The paraplegia did not improve and the pa- tient was transferred to the Toronto Western Hospital. On arrival, the complete paraplegia was still present. There was no motor or sensory function below T-10. The rest of the examination was unremarkable. The CT scan, myelogram, and abdominal ultrasound study were reviewed and considered to be normal. The clinical diagnosis was spinal cord infarction or hemorrhage. Treatment in the hospital included dexamethasone, 4 rag, administered intravenously every 6 hours and 938 J. Neurosurg. / Volume 71/December, 1989