How Cortical Spreading Ischemia leads to DCI

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  • cortical neuronal swelling
  • dendrite spine distortion
  • slow changes in brain electrical potential (spreading depolarization)
  • decreased brain electric activity (spreading depression)

Normal Neurovascular Coupling:  Spreading depolarization –> arterioles vasodilate –> hyperemia –> no permanent damage

Abnormal Response:  Spreading depolarization –> inc astrocyte calcium and activation of calcium-activated potassium channels –> arterioles constrict –> waves of cortical hypoperfusion or cortical spreading ischemia

How does this happen?  sodium and calcium influx through multiple ion channels –> loss of electrically negative intraneuronal state –> spreading depolarizations –> prevents action potential formation –> propagates as a wave across cortex –> neurons lack adequate energy supplies to re-establish transmembrane ionic gradients –> cortical spreading ischemia

Subdural strip electrodes studies:

  • 70% of SAH aptients have repetitive cortical spreading depolarizations
  • some patients developed DCI that was spatially and temporally associated with angiographic vasospasm and cortical spreading depolarization
  • patients who had depolarization lasting >60minutes developed infarction on CT or MRI

Cortical spreading ischemia after SAH can be inhibited by nimodipine, NMDA receptor antagonists and prevention of systemic volume depletion

Reference

Macdonald, R. Loch. “Delayed Neurological Deterioration After Subarachnoid Haemorrhage”. Nature Reviews Neurology 10.1 (2013): 44-58.

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