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Maturation Phenomenon in Cerebral Ischemia III - Defensive Mechanisms Versus Apoptosis Neuronal Recovery and Protection in Cerebral Infarction (Paperback, illustrated edition)
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Maturation Phenomenon in Cerebral Ischemia III - Defensive Mechanisms Versus Apoptosis Neuronal Recovery and Protection in Cerebral Infarction (Paperback, illustrated edition)
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The Maturation Phenomenon, described by Ito et al. in 1975 [3) on
the basis of his to logical observations in the hippocampus as well
as other portions of the cerebral hemisphere, refers to the hours
or days of delay in the development of pathological changes in
various parameters of ischemic injury following the restoration of
blood flow to the ischemic brain. There is a direct relationship
between the intensity of ischemic insult and the speed and rate of
maturation of ischemic injury, a lesser intensity being associated
with slower and less severe development of the lesions. The delayed
neuronal death of CAl pyramidal cells of the hippocampus [8) is a
classic example. In the cerebral cortex, with increasing intensity
of the ischemic insult, the maturation phenomenon of ischemic
injuries intensifies, seamlessly, from less exten sive to more
extensive disseminated selective neuronal necrosis (DSNN), and then
further to cerebral infarction upon reaching a critical threshold
[1,2,4,6,7). We also have found that following ischemic insults
just under the threshold level required to induce infarction, only
disseminated selective neuronal necrosis (DSNN) progresses, while
following ischemic insults at the threshold level, initially only
DSNN develops, followed by the evolution of a gradually enlarging
infarcted focus [5, 7). The reporting of this phenomenon boosted
research in the field, as it became evi dent that ischemic damage
is not a sudden event, but a process potentially susceptible to
therapeutic intervention.
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