As I learn more and more about CNS O2 toxicity, I become less and less
convinced that accumulated "dose" (i.e., prior exposure) has much
influence
on probability of convulsion.

I really think Rich is correct here.
My gut feeling, confirmed by review of the relevant diving medicine and
neurology texts, is that the symptoms of acute CNS oxygen toxicity are
the same as transient global cerebral ischemia.
OK, I'll translate-
The brain protects itself from oxygen poisoning by reducing the flow of
blood to the brain.  When you reduce the flow of blood to the brain, you
get:  dizziness, blacking out of vision, loss of hearing, loss of
consciousness, and convulsions.  This is probably due to a sudden loss
of glucose to the brain cells and a rapid build up of toxins in the
brain.  This happens when people faint also.
So basically, its not the amount of oxygen that you've been exposed to,
nor the pPO2 per se, but rather the way your brain is reacting.  This
would explain why there is so much variability in a given individual and
especially between individuals when it comes to O2 seizures.
If this is true, it would help to explain why WKPP people can exceed
"standards" without any adverse effects.
I'll stop before going on with my thoughts on why pulmonary toxicity
needs to be reassessed in the light of current real dive data.
Wendell Grogan
--
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