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  • Author or Editor: Richard B. Morawetz x
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Mark J. Cuffe, Mark N. Hadley, Guillermo A. Herrera and Richard B. Morawetz

✓ Ten patients undergoing long-term renal dialysis for end-stage renal failure developed a destructive, noninfectious spondylarthropathy. All 10 patients had biopsy-proven dialysis-associated spondylarthropathy and subsequent spinal instability secondary to beta 2-microglobulin deposition in the vertebrae, intervertebral disc spaces, and support structures of the spine. Nine patients had cervical spinal instability and one had thoracolumbar spinal instability, with resultant neural compression. In at least one patient, the spinal instability was rapidly progressive. All had received renal dialysis for 34 months or longer (mean 109 months, range 34 to 154 months). Each patient required spinal stabilization (external in seven patients, internal in three). Nine of the 10 patients underwent neural decompression and spinal stabilization and fusion procedures.

One patient's neurological condition was worse following surgery due to a postoperative cervical epidural hematoma; in the other nine patients, the presenting symptoms and signs improved. Three of these chronically ill patients did not survive their hospitalization, for a perioperative mortality rate of 30%. Death was due to cardiopulmonary arrest in two patients on Day 5 and 9 postoperatively and to sepsis in the third on Day 14. Of the seven early survivors, two additional patients died: one on Day 59 due to congestive heart failure and the other on Day 273 due to a cerebrovascular accident. Four of five patients who were followed for 8 months or longer (mean 14 months, range 8 to 20 months) had successful neural decompression and spinal stabilization procedures with evidence of stable bone fusion, indicating that these chronically ill, difficult-to-manage patients can be successfully treated. Clinicians who treat patients with renal disease and neurosurgeons who treat spinal disorders should be aware of dialysis-associated spondylarthropathy as a potential cause of degenerative vertebral column instability.

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Thomas H. Jones, Richard B. Morawetz, Robert M. Crowell, Frank W. Marcoux, Stuart J. FitzGibbon, Umberto DeGirolami and Robert G. Ojemann

✓ An awake-primate model has been developed which permits reversible middle cerebral artery (MCA) occlusion during physiological monitoring. This method eliminates the ischemia-modifying effects of anesthesia, and permits correlation of neurological function with cerebral blood flow (CBF) and neuropathology. The model was used to assess the brain's tolerance to focal cerebral ischemia. The MCA was occluded for 15 or 30 minutes, 2 to 3 hours, or permanently. Serial monitoring evaluated neurological function, local CBF (hydrogen clearance), and other physiological parameters (blood pressure, blood gases, and intracranial pressure). After 2 weeks, neuropathological evaluation identified infarcts and their relation to blood flow recording sites.

Middle cerebral artery occlusion usually caused substantial decreases in local CBF. Variable reduction in flow correlated directly with the variable severity of deficit. Release of occlusion at up to 3 hours led to clinical improvement. Pathological examination showed microscopic foci of infarction after 15 to 30 minutes of ischemia, moderate to large infarcts after 2 to 3 hours of ischemia, and in most cases large infarcts after permanent MCA occlusion. Local CBF appeared to define thresholds for paralysis and infarction. When local flow dropped below about 23 cc/100 gm/min, reversible paralysis occurred. When local flow fell below 10 to 12 cc/100 gm/min for 2 to 3 hours or below 17 to 18 cc/100 gm/min during permanent occlusion, irreversible local damage was observed.

These studies imply that some cases of acute hemiplegia, with blood flow in the paralysis range, might be improved by surgical revascularization. Studies of local CBF might help identify suitable cases for emergency revascularization.

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H. Evan Zeiger Jr., Edward J. Zampella, David C. Naftel, Robert D. McKay, Pamela D. Varner and Richard B. Morawetz

✓ Carotid endarterectomy may carry a substantial risk of morbidity and mortality from major stroke, thus offsetting any statistical benefit in reduction of future stroke. Because of the disturbing ranges in the incidence of stroke morbidity and mortality reported from the several institutional series studying carotid endarterectomy, the authors undertook a prospective review of 142 consecutive carotid endarterectomies performed for symptomatic atherosclerotic occlusive vascular disease on the neurosurgical service, The University of Alabama Hospital. Preoperative risk assessment was performed in each case according to the Mayo Clinic classification system. The overall mortality rate was 1.4% and the major stroke morbidity rate was 0.7%, for a combined major morbidity and mortality rate of 2.1%. The incidence of minor neurological morbidity was 1.4%. There was no morbidity or mortality in the Grade I and II (low-risk) patient groups. This low combined major morbidity and mortality rate of 2.1% for carotid endarterectomy causes the surgical stroke-free survival curve to intersect the medical stroke-free survival curve at an earlier point in time, and thus demonstrates the greater reduction in risk of stroke which accrues over time for the surgically treated patient.

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Edward J. Zampella, Ernest R. Duvall, B. Chandra Sekar, Keith H. Langford, Andrew E. Epstein, James K. Kirklin and Richard B. Morawetz

✓ Patients with Cushing's syndrome may develop spinal epidural lipomatosis, an abnormal accumulation of fat in the spinal epidural space. This accumulation of fat may cause compression of the spinal cord or cauda equina with resulting neurological deficit. Two cases of symptomatic spinal lipomatosis are reported in cardiac transplant patients receiving chronic corticosteroid treatment. The literature is reviewed, and diagnostic and therapeutic considerations are discussed.