Concept and pathogenesis of "hypoxic-ischemic encephalopathy".

By experiments of acute carbon-monoxide intoxication, acute nitrogen hypoxia and histotoxic hypoxia using sodium cyanide in cats, and by hemodynamic studies using plastic branch models, the following was elucidated; (1) severe tissue hypoxia, regardless of the underlying cause, and subsequent slight ischemia of the brain due to mild hypotension induce selective involvement of the cerebral white matter and pallidum, these two conditions being necessary and sufficient and this encephalopathy should be separately categorized as "hypoxic-ischemic encephalopathy" in hypoxic brain injuries, (2) the background of the selective involvement of these structures is an enormous development of the cerebrum in the brain, which induces thick white matter resulting in proper and long medullary artery, and especially small diameter ratio of the pallidal perforators to the middle cerebral artery, (3) the long course of the medullary artery produces the blood pressure drop in the deep white matter according to Hagen-Poiseuille's low, and according to that the smaller the diameter ratio, the larger the branching-loss coefficient (energy-loss co-efficient), smaller diameter ratio of the pallidal perforator, as compared with that of the putaminal perforator, induces more severe loss of the local blood flow selectively to the pallidum. This state seems to be a failure of compromise between the cardiovascular system and the brain parenchyma.