GV. Sparacia, B. Sparacia, A. Sansone

In treating encephalic lesions with hyperbaric oxygen our experience springs from over a decade's descriptions by various authors who worked at appraising feasible therapies using it in experience both clinical and experimental (3,4,5,6,7,9). Recalling the ischemic penumbra zone's physiopathology, HBO administration offers a restriction of post-ischemic perfusional damage both directly through improved bio-availability of oxygen in ischemic areas, and indirectly through regulatory action of cerebral flow that improves perfusion in "critical" areas. Without dwelling on the problems of metabolism and perfusion that follow cerebral lesions, we can take for certain that:

• HBO improves oxygen diffusibility both above and beneath tentorial level, encouraging in affected areas metabolic and ATP action by lowering lactates and raising ATP (2,3,7);
• Improves glucose metabolisation by lowering production of substances, like aspartate and glutamate, responsible for over-response of the receptors (2);
• Due to improved metabolic processes and well-timed perfusional flow redistribution with suitably controlled treatment, the generation of radicals in the intracranial area is brought under greater control;
• As therapy can act only on areas not irreversibly damaged (1), treatment must occur as early as possible
  Indeed it is the bringing of dissolved oxygen up to glial level that is truly the new fact to be attributed to HBO in treating brain damage. And precisely where the phenomenon of blood redistribution from non-ischemic areas to tissues around the lesions is to be taken into account, which is affected by the vasoconstriction effect to which unharmed areas are notoriously more susceptible, with evident result lowering, "stealing" and intracranial pressure and raising tissue oxygen flow.

Bibliography:

1. Dir R.C., Faiman M.D.: "Free radical formation and lipid peroxidation in rat and mouse cerebral cortex slices exposed to high oxygen pressure." Brain Res. 248, 355 1982
2. Gelmers HI.: "New aspects of stroke therapy." Int Sym Calcium Antagonist. New York; feb.1988.
3. Kovachich G.B., Miahara O.P., Clark G.M.: "Depression of cortical Na/K/ATPasi activity in rats exposed to hyperbaric oxygen." Brain Res. 206,229 1981
4. Nakajama S., Meyer J.S., Amato T., Shaw T., Okabe T., Mortel K.F.: "Cerebral vasomotor responseness during 100% Oxygen inhalation in cerebral ischemia." Arc. Neurol. 40,27, 1983.
5. Neubauer R.A.: "Regional blood flow studies of the effect of HBO in acute stroke neurologic deficits in 30 cases." Seventh Annual Conf. on Clinical Appl. of HBO. Anaheim CA. June 1982
6. Paulson in Neubauer R.A.: "Hyperbaric oxygen therapy of stroke." A. Review. Landerdale by the sea. Florida USA 1983 7) Shiokawa O., Fujishima M., Yuoi T., Ibayashi S., Yagi H.: "Hyperbaric oxygen therapy in experimentally induced acute cerbral ischemia." Undersea biomedical research 13,3, 337 1986.