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RE: [IP] good A1Cs without frequent lows possible? (Brain damage)

Thank You Bob. That is exactly what I was looking for. Now I have to choose
weather to have complications from being to low or being to high. I guess
that is part of being Diabetic. I am not a normal non diabetic and probably
will never be. Just have to try to get to normal numbers the best way I can,
even when it means I subject myself to problems I can't control.

Have A Good Day
John S Wilkinson
Rome, New York

-----Original Message-----
From: email @ redacted
[mailto:email @ redacted] On Behalf Of Bob Kerns
Sent: Thursday, May 11, 2006 7:40 AM
To: email @ redacted
Subject: RE: [IP] good A1Cs without frequent lows possible? (Brain damage)

First, some historical perspective from 20 years ago:

[Stroke. 1986 Jul-Aug;17(4):699-708.]

Progress review: hypoglycemic brain damage.

Auer RN.

 The central question to be addressed in this review can be stated as "How
does hypoglycemia kill  neurons?" Initial research on hypoglycemic brain
damage in the 1930s was aimed at demonstrating the  existence of any brain
damage whatsoever due to insulin. Recent results indicate that uncomplicated
hypoglycemia is capable of killing neurons in the brain. However, the
mechanism does not appear to  be simply glucose starvation of the neuron
resulting in neuronal breakdown. Rather than such an  "internal catabolic
death" current evidence suggests that in hypoglycemia, neurons are killed
from  without, i.e. from the extracellular space. Around the time the EEG
becomes isoelectric, an  endogenous neurotoxin is produced, and is released
by the brain into tissue and cerebrospinal fluid.  The distribution of
necrotic neurons is unlike that in ischemia, being related to white matter
and  cerebrospinal fluid pathways. The toxin acts by first disrupting
dendritic trees, sparing  intermediate axons, indicating it to be an
excitotoxin. Exact mechanisms of excitotoxic neuronal  necrosis are not yet
clear, but neuronal death involves hyperexcitation, and culminates in cell
membrane rupture. Endogenous excitotoxins produced during hypoglycemia may
explain the tendency  toward seizure activity often seen clinically. The
recent research results on which these findings are based are reviewed, and
clinical implications are discussed.
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