Progress review: hypoglycemic brain damage.

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