Neurologic damage in hypoglycemia

作者: Simin Mohseni

DOI: 10.1016/B978-0-444-53480-4.00036-9

关键词:

摘要: Hypoglycemia occurs in diabetic patients as a consequence of treatment with hypoglycemic agents, insulinoma result excessive insulin production, and infants abnormal regulation metabolism. Profound hypoglycemia can cause structural functional disturbances both the central (CNS) peripheral nervous system (PNS). The brain is damaged by short severe episode hypoglycemia, whereas PNS pathology appears after mild prolonged episode. In CNS, mitochondria, elevated intracellular Ca2(+) level, released cytochrome c to cytosol, extensive production superoxide, increased caspase-3 activity, release aspartate glutamate from presynaptic terminals, altered biosynthetic machinery lead neuronal cell death brain. Considering PNS, chronic associated delayed motor sensory conduction velocities nerves. With respect pathology, neuropathy characterized Wallerian-like axonal degeneration that starts at nerve terminal progresses more proximal part axon, axons muscles may be severely than axons. Since excitatory neurotransmitters primarily involve neuron this "dying back" pattern damage mechanisms other excitotoxicity.

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