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Washington University Experience | VASCULAR | Infarct - Spinal Cord | 4A0 Case 4 History
Case 4 History ---- The patient was a 52 year old man with a past medical history significant for hypertension, chronic alcoholism, and a history of seizures (thought to be alcohol related) who expired on 8-14, 25 days after admission for acute quadriparesis. The patient was reportedly in his usual state of health until several days prior to admission at which time he complained of generalized "weakness". His neighbors did not see him leave his house for several days and eventually checked on him, finding him lying in bed unable to move. On initial evaluation he was noted to be alert but fairly uncooperative and confabulating. He had bilateral flaccid weakness in all extremities and a mid-cervical sensory level. He had upgoing toes bilaterally. He had an MRI scan of the cervical and thoracic spine which demonstrated severe spondylolysis with large disc bulge associated with osteocyte formation and cord compression at the C3-4 and C4-5 levels and moderate spinal stenosis also seen at the C5-6 level. These changes were associated with high T2 signal within the spinal cord from C2 to C6, felt to represent edema vs. gliosis. An urgent decompressive laminectomy was performed on 7-21 with no change in neurologic status. He required re-intubation later the same day for respiratory distress. From a neurologic standpoint, the patient's condition remained unchanged following his cervical decompression. He continued to have a neurogenic bladder and bowel, as well as paralysis in all four extremities with the exception of some movement in the left deltoid. He maintained a C4 sensory level. The remainder of his hospital course was essentially one of progressive respiratory decline, infection with a resistant pseudomonas organism and fever. He had difficulties with episodes of decreased O2 saturations and was found apneic and pulseless on 8-14 and was not resuscitated. ---- At autopsy a mid-cervical level infarct was discovered in the presence of general hyalinization of parenchymal cord blood vessels. Although the reason for this patient’s sudden neurologic decline is not clear by history, the spinal cord infarct most likely resulted from long-standing, severe spondylolysis/spinal stenosis which had been progressive, followed by some type of more acute injury. In view of the extensive degenerative changes by imaging prior to his surgery, the vascular supply to his spinal cord was likely tenuous at best and even minimal additional compromise could have resulted in the subsequent cord infarct.
