1/61. Painful tonic/dystonic spasms in sjogren's syndrome. Three patients with sjogren's syndrome are presented in whom frequent tonic/dystonic spasms of the limbs developed during the course of the illness. These patients' clinical findings suggested spinal cord involvement, a localization that was confirmed by magnetic resonance imaging in two patients. In one patient the painful movements responded to treatment with phenytoin and in one other to baclofen. sjogren's syndrome should be considered in the differential diagnosis of conditions that produce tonic/dystonic limb spasms. ( info) |
2/61. Evoked spinal cord potential monitoring reveals peroneal nerve ischemia during thoracoabdominal repair: a case report. An 82-year-old man underwent thoracoabdominal aortic replacement under cardiopulmonary bypass with left femoral artery cannulation. Lumber descending evoked spinal cord potentials and segmental evoked spinal cord potentials were monitored simultaneously for detecting spinal cord damage. When the cardiopulmonary bypass was terminated, a peripheral nerve ischemia pattern was evident. Left peroneal nerve paralysis was present at emergence from anesthesia. This monitoring system revealed that peroneal nerve paralysis can occur due to leg ischemia caused by femoral artery cannulation. This is, to our knowledge, the first report that segmental evoked spinal cord potential monitoring reveals peroneal nerve ischemia during thoracoabdominal surgery. ( info) |
3/61. Reversible ischemic myelopathy during scoliosis surgery: a possible role for intravenous lidocaine. An unusual and previously unreported case of partially reversible ischemic myelopathy after limited unilateral segmental vessel ligation during scoliosis surgery is described. Intravenous lidocaine, used intraoperatively for its vasoactive properties, induced an immediate and meaningful recovery of neurologic function. The conceptual and pharmacologic basis for this intervention is discussed in view of this exceedingly rare complication of segmental vessel ligation. ( info) |
4/61. Reversal of twice-delayed neurologic deficits with cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a national database collection. Delayed neurologic deficits are an uncommon yet devastating complication of thoracoabdominal aortic aneurysm repair. The mechanisms involved in the development of delayed spinal cord ischemia remain ill defined. We report a case of complete reversal of delayed neurologic deficits with postoperative cerebrospinal fluid (CSF) drainage. After a thoracoabdominal aneurysm extent I repair, the patient experienced delayed paraplegia at 6 hours and again at 34 hours after the operation, with elevated CSF pressure (>10 mm Hg) on both occasions. Prompt CSF decompression completely reversed the neurologic deficits within hours after onset. The findings in this case further support the role of CSF drainage in spinal cord protection for patients who undergo thoracoabdominal aneurysm repair and make a plea for a national database collection. ( info) |
| PURPOSE: To report a case of endovascular descending thoracic aortic aneurysm (TAA) repair in which delayed-onset paraplegia was reversed using cerebrospinal fluid (CSF) drainage. methods AND RESULTS: A 74-year-old patient with a 6.0-cm TAA underwent endovascular stent-graft repair that involved overlapping placement of 3 Talent devices to cover the 31-cm-long defect. Twelve hours later, a neurological deficit occurred manifesting as left leg paralysis with paresis on the right. After urgent intrathecal catheter placement and drainage of cerebrospinal fluid for 48 hours, the neurological deficit resolved. The patient's clinical condition was normal and endoluminal exclusion of the TAA remained secure at 8-month follow-up. CONCLUSIONS: This case demonstrates the potential therapeutic role for CSF drainage to reduce the complications of spinal cord injury after endovascular thoracic aneurysm repair. ( info) |
6/61. Spinal cord infarction and tetraplegia--rare complications of meningococcal meningitis. A previously healthy 25-yr-old female developed flaccid areflexic tetraplegia, with intact cranial nerve function, 36 h after the diagnosis of bacterial meningitis. polymerase chain reaction studies of cerebrospinal fluid and blood were positive for neisseria meningitidis, serogroup b. Magnetic resonance of the cervicothoracic spine revealed increased signal intensity and expansion in the lower medulla, upper cervical cord and cerebellar tonsils. Neurosurgical consultation recommended hyperventilation, dexamethasone and regular mannitol therapy rather than decompressive intervention. The clinical course over the following 12 days was complicated by the development of progressive central nervous and multisystem organ failure with disseminated intravascular coagulopathy. autopsy revealed cerebral oedema with cystic infarction extending from the medulla to the upper cervical cord and cerebellar tonsils. Flaccid areflexic tetraplegia with spinal cord infarction has not been reported following bacterial infection in an adult. The clinical implications would suggest complete central nervous system evaluation of patients recovering from meningococcal meningitis, since spinal cord lesions, although uncommon, do occur. In those very rare situations where a patient develops significant peripheral neurological deficits, urgent magnetic resonance imaging is warranted, to rule out an infective focus or an underlying anatomical anomaly. ( info) |
7/61. Vertebral artery anomaly with atraumatic dissection causing thromboembolic ischemia: a case report. STUDY DESIGN: A case report is presented. OBJECTIVES: To illustrate a rare cause of atraumatic vertebral artery dissection resulting from anomalous entry of the vessel at the C3 transverse foramen induced by normal physiologic head and neck motion, and to review vertebral artery anatomy and mechanisms whereby it is vulnerable to pathologic compression. SUMMARY OF BACKGROUND DATA: The vertebral artery usually enters the transverse foramen at C6. Rarely, the artery enters at C5 or C4. Only one prior case with entry at C3 has been reported. That patient experienced recurrent quadriplegia and locked-in syndrome caused by vertebral artery obstruction. A 27-year-old woman with a history of classic migraine experienced neurologic symptoms on three occasions related to physiologic neck and arm movements. Magnetic resonance angiogram was not diagnostic, but standard arteriography demonstrated anomalous vertebral artery entry into the C3 transverse foramen and focal dissection. methods: Pertinent literature and the patient's history, physical examination, and radiologic studies were reviewed. RESULTS: Standard cervico-cerebral arteriogram demonstrated focal dissection at C4 and thromboembolic complications in distal vertebral and basilar arteries. Initially, diagnosis by magnetic resonance angiogram was elusive. However, arteriography allowed prompt diagnosis followed by anticoagulation with resolution of neurologic symptoms. CONCLUSIONS: vertebral artery dissection without trauma is rare, but should be considered when neurologic symptoms accompany physiologic cervical movements. For cases in which vertebrobasilar thromboembolic ischemia is suspected, magnetic resonance angiogram may prove inadequate for demonstrating the causative vascular pathology. Therefore, standard cervico-cerebral arteriography should be performed. ( info) |
8/61. Spinal cord infarction following vertebral angiography: clinical and pathological findings. Spinal cord damage from radiographic contrast material has been known to occur in both spinal and nonspinal angiographic procedures. Reported here is cervical spinal cord injury (SCI) during vertebral angiography. During the procedure, the patient displayed signs of acute cervical spinal cord irritation that should have been taken as a warning of impending injury. autopsy 9 years later showed evidence of central cervical spinal cord necrosis. The pathological findings are similar to those seen in animal models of contrast media-induced SCI; and the pathophysiological mechanisms of such injury are discussed. ( info) |
9/61. Lumbar artery compression by the diaphragmatic crus: a new etiology for spinal cord ischemia. We describe a new cause of spinal cord ischemia illustrated by two cases--compression by the diaphragmatic crus of a lumbar artery giving rise to a spinal artery. The diagnosis has been established by dynamic spinal angiography, showing complete occlusion of the lumbar artery. Surgical section of the diaphragmatic crus prevents irreversible infarction. ( info) |
10/61. Neuropathic pain syndrome as an occult manifestation of injury of the spinal cord after surgical repair of aortic coarctation. Injury to the spinal cord injury with paraplegia, is a rare complication of surgical repair of aortic coarctation recognized immediately post-operatively. We present the case of a 41-year-old male undergoing surgery for restenosis at the site of a repair. Intra-operatively, he suffered inadvertent injury to an intercostal arterial branch during isolation of the aorta below the graft. Over the following months, he developed unusual symptoms involving the legs and genitourinary tract which, only after extensive investigations, were attributed to ischemic damage to the spinal cord related to the surgery. We suspect that similar syndromes reflecting injury to the spinal cord injury may be unrecognized following surgical repair of coarctation. ( info) |