✓ A family with craniofacial dysostosis affecting a father and his monozygotic twin sons is described. The father had no surgery until linear craniectomy when 3 years old; he is of normal intelligence but legally blind. Prophylactic coronal craniectomy and orbital decompression were done on the twins. One had an uncomplicated course and is developing normally. The other developed neonatal meningitis and ventriculitis with secondary hydrocephalus, plus poor vision and retarded development.
Jane C. S. Perrin, Martin H. Weiss and David Yashon
David Yashon, Robert J. White, Belisario A. Arias and William E. Hegarty
✓ Some intracranial aneurysms, because of their broad base or incorporation of essential nutritive vessels, must be treated by adhesive reinforcement. The authors report successful results with cyanoacrylate adhesives in five patients. The unique quality of this material permits maximum adhesion in a moist operative field. This adhesive is nonviscous and will coat the entire aneurysm, obviating problems related to incomplete coating. Excellent long-term results are apparently due to the biological effect of this adhesive in which a proliferative fibrous reaction occurs and counteracts recognized erosive properties.
George E. Locke, David Yashon, Robert A. Feldman and William E. Hunt
✓ Lactate accumulation in spinal cord tissue following trauma was determined to ascertain the role and magnitude of ischemia. High thoracic and low thoracic laminectomies were performed on each of nine rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. The upper exposed cord served as a nontraumatized control. At time intervals of 1.5 min to 48 hrs after trauma, both cord segments were removed and assayed for lactic acid. Lactate in nontraumatized segments averaged 3.64 mM/kg tissue, with a range of 2.20 to 4.95. Lactate in traumatized segments removed in from 1.5 min to 12 hrs from six monkeys averaged 5.50 mM/kg tissue, with a range of 4.32 to 6.46. Lactate in traumatized segments from three monkeys 18 to 40 hrs after trauma averaged 4.07 mM/kg, with a range of 3.20 to 5.18. This finding supports the concept that ischemia plays a role early in the traumatic process in spinal cord injury.
Robert A. Feldman, David Yashon, George E. Locke and William E. Hunt
✓ In rhesus monkeys subjected to circulatory arrest, studies were made of the relationship of lactate production in the spinal cord to the duration of circulatory arrest and magnitude of lactate accumulation, and the results were compared to the magnitude of rise in cerebral tissue lactate. Both high and low thoracic laminectomies were performed on each of eight rhesus monkeys. Spinal cord tissue was excised for lactate assay at the upper laminectomy as a control, and a second tissue specimen was excised at the lower laminectomy site at time increments of 30 sec to 30 min after circulatory arrest. Tissue was excised from each site without circulatory arrest in one monkey and showed negligible increase in lactate production, indicating that excision of tissue itself does not result in increased lactate. Nonanoxic samples from seven monkeys averaged 4.60 millimoles (mM)/lactate/kg tissue, with a range of 2.22 to 6.49. Postcirculatory arrest samples from these monkeys averaged 11.10 mM lactate/kg tissue, with a range of 3.62 (at 30 sec) to 14.33 (at 10 min). Anoxic spinal tissue lactate was elevated above controls in each instance, and tissue lactate peaked between 5 to 10 min after circulatory arrest and remained stable with mild fluctuations beyond that time. Thus, the spinal cord responds to circulatory arrest much as cerebral tissue, but with some delay in the accumulation of lactic acid.
David Yashon, George E. Locke, W. George Bingham Jr., Wigbert C. Wiederholt and William E. Hunt
✓ Electrocortigraphic activity and common carotid blood flow were studied in 12 dogs during and following profound oligemic hypotension. Five animals survived but seven died within 75 min of hypotension. Although an 80% to 90% reduction in both mean arterial pressure and common carotid blood flow was observed, only a 20% diminution of intracranial pressure occurred and there was little change in electrocorticographic function. The preservation of cerebral function in the presence of profound systemic hypotension was demonstrated. When death occurred during shock, no prior change in central nervous system function was noted. With reinfusion, no change in parameters was noted, but common carotid blood flow was depressed to 35% to 50% of control levels for up to 2½ hrs of observation.