What causes infarction in ischemic brain?: The Robert Wartenberg Lecture

Neurology. 1983 Feb;33(2):222-33. doi: 10.1212/wnl.33.2.222.


Improved treatment of associated cardiovascular and hematogenous abnormalities has favorably influenced the incidence and outcome of cerebral vascular disease during the past 25 years. Strong evidence now indicates that attention to the carbohydrate content of the brain also may influence outcome from brain ischemia. With brain lactate levels above approximately 16 mmol per kilogram, ischemia produces tissue infarction; ie, the lesion includes astrocytic and endothelial necrosis as well as neuronal death. We find that equal degrees of ischemia accompanied by lower tissue lactate values produce only selective neuronal damage in predictably vulnerable areas; astrocytes and endothelia are spared and extracellular or progressive postischemic cerebral edema fails to develop. The findings suggest that astrocytes can function to defend brain tissue against the damaging effects of acute anoxia but that during such conditions, they are potentially vulnerable to high tissue lactate levels. Initial clinical evidence suggests that scrupulous attention to blood sugar may reduce the risk of human cerebral infarction after ischemia.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Astrocytes / ultrastructure
  • Blood Glucose / analysis
  • Cerebral Infarction / blood
  • Cerebral Infarction / etiology*
  • Cerebral Infarction / physiopathology
  • Humans
  • Hypoxia, Brain / complications
  • Hypoxia, Brain / physiopathology
  • Ischemic Attack, Transient / blood
  • Ischemic Attack, Transient / complications*
  • Ischemic Attack, Transient / pathology
  • Ischemic Attack, Transient / physiopathology
  • Lactates / blood
  • Neurons / pathology


  • Blood Glucose
  • Lactates