Cerebral oedema represents the main aggravating factor to be predicted in various forms of brain ailments. Oedema is initially produced at a threshold of cerebral blood flow (CBF) lower than 20 ml/100 gr/min., so an early stage of cytotoxic oedema is followed by a vasogenic-oedema stage coincident with reperfusion.

     After reperfusion circulatory and metabolic changes persist in the period following ischemic attack, yet the brain metabolism's special nature makes the neuronal cell more resistant to hypoxia than was previously supposed by clinical experience. Most of the ischemic penumbra zones may thus make a full recovery if appropriate therapy is applied at the right time. Consideration of this kind have led to proposals of various therapies all with the scope of lowering brain consumption of O₂, improving perfusion in the brain and relieving nerve tissue from all mechanical pressure. However, no suggested treatment seems without disadvantages and risks, so there is no agreed consensus of opinion. Actually the only effective treatment, in having no contra-indications or paradoxical results, seems to be mechanical ventilation with timely checks on PaCO₂ values.

     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 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.

    It logically follows - as epiphenomenon of what we sketched out, and subject matter of our previous notes - our aim is reduction of oedema and of PIC with overall improvement of cell perfusion. We always gave prominence to testing clinically how useful a tool HBO may be in conjunction with conventional treatments by now applied everywhere, assessing results so as to suggest conditions where such treatment might be indeed effective and where, on the contrary, useless or, worse, contra-indicated. Without dwelling on the problems of metabolism and perfusion that follow cerebral lesions, we can take for certain that:

a) 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);

b) improves glucose metabolisation by lowering production of substances, like aspartate and glutamate, responsible for     over-response of the receptors (2);

c) 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;

d) as therapy can act only on areas not irreversibly damaged (1), treatment must occur as early as possible;

e) HBO's antioedemigenic action, though theoretically of the greatest use, however needs active support therapy to     avoid or check risks of rebound effects, by planning different treatment cycles together with precise     morpho-functional monitoring of  the encephalon.

In line with our experience of nearly 4 years we thought it especially useful to study HBO's effects on subjects with focal brain damage involving (or not) altered consciousness states due to ischemia, thrombosis and/or having a  small site of haemorrhage not relevant to neurosurgery but leading in any case to an asymmetry of measured flow between the to hemisphere, but excluding:

a) generalised cerebral oedema and practically irreversible damage;

b) subjects with high level of carotid stenosis.

For comparative data we used morphofunctional features and their development, metabolic features connected with brain oxygen flow, and finally the prognosis of possible improvement both quoad vitam for life quality and in relation to the results. So monitoring was by means of: CT at admission and 6 hours after first treatment, then every 24-36 hours; auditory and somatosensory evoked potentials every 8 hours; EEG 3 hours after end of treatment; Echo-Doppler of epiaortic vessels at admission and after HBO therapy; haemogasanalysis; Glasgow Coma Scale; CMRO₂ assessment and, where possible, measurement of liquor pressure by lumbar puncture before and 3 hours after wards.

Lastly, brain bloodflow measure with INHAMATIC 33 SYSTEM (Medimatic) 6 hours after first treatment, repeated 24 hours later. In line with this plan 26 subjects of both sexes, aged between 48 and 64, were studied: patients admitted to our Reanimation Centre for encephalic disorders of vascular or traumatic origin (Table 1), divided into 2 groups of 13 patients each: the first (Group A), after we had consent, were given HBO in conjunction with usual therapies. HBO treatment was applied with bathymetry of 1.5-1.8 ATA for 66 minutes subdivided into three 20 minute oxygen-breathing cycles (FiO₂ = 1) using facial mouth-mask or intubation in the trachea and mechanical ventilation, with 3 minute intervals of air breathing. Treatment was repeated every 12 hours for the first 4 days, then at daily intervals for 8-10 days. The second group was treated instead with routine therapies (either for absence of consent or because of late transfer from other departments) and taken as control (Group B). data are given as mean + DS. Statistical analysis was made using variance analysis for multiple values (ANOVA).

Table 1

Commenting straightaway on these data, there is clearly lower death-rate, though not significant, in subject treated with HBO, just as function recovery is also favoured, both morphological aspects and metabolic (CNRO₂) and clinical (CGS) ones. On the other hand, improved prognosis is dramatically higher both for life quality/quoad vitam and for functioning, in the patient group in post-traumatic coma, with or without focus-site lesions. This is effective therapeutics, confirmed by improved evoked potential responses but mainly by measured bloodflow data that always showed a tendency to redistribute and homogenise flow, with vasoconstriction persisting at the check after 6 hours.

There was no case of increased oedema around the lesion after treatment nor diametrical growth of focus-site. Summing up, in agreement with the most recent biochemical, clinical and therapeutic observations already reported in connexion with post-anoxic brain lesion treatment (8), HBO's usefulness can be confirmed, as long as it is applied rigorously with suitable monitoring, even for ever more refined researches into phisiopathology and brain damage. Improved perfusion treatment plus activating of inverse haematic (stealing" phenomenon and oxygen bioavailability brought into penumbra area, all explain the positive effects on metabolism of nerve-cells and glia, lowering or eliminating oedemigenic effects of a histotoxic and angiogenic kind, with outcomes visible with CT and bloodflow measurement.

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

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.

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