Pathomechanism of Hypoxic Ischemic Neuronal Necrosis

Hypoxic-ischemic neurons die of the excitotoxic effects of the neurotransmitter glutamate and its analogs that accumulate in excess in ischemic tissue. These excitatory neurotransmitters depolarize the neuronal membrane, allowing excessive influx of sodium, chloride, water, and calcium into the neuronal compartment. Subsequent swelling, metabolic dysfunction, and disruption of the cellular membrane ultimately lead to the disintegration of the neurons.

Why neurons in certain regions are more vulnerable to hypoxia-ischemia than are those in other regions has not been elucidated fully. Regional differences in vascular architecture seem not to be a satisfactory explanation. Regional differences among neurons possessing specific receptors for locally released excitatory neu-rotransmitters are a more likely explanation. Hence, regions with the highest concentration of neurons that possess glutamate-sensitive receptors are the most vulnerable to hypoxia-ischemia.

FIGURE 3.6

Hypoxic-ischemic leukoencephalopathy. Twelve days prior to his death, a 66-year-old man with chronic obstructive lung disease suffered a severe acute exacerbation, which failed to respond to intensive therapy. Macrosection from the cerebral hemisphere shows small focal areas of myelin pallor (LFB-HE).

FIGURE 3.6

Hypoxic-ischemic leukoencephalopathy. Twelve days prior to his death, a 66-year-old man with chronic obstructive lung disease suffered a severe acute exacerbation, which failed to respond to intensive therapy. Macrosection from the cerebral hemisphere shows small focal areas of myelin pallor (LFB-HE).

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