Experimental hypoxic brain damage.

The majority of hypoxic episodes that result in histologically proven damage in the human brain cannot be adequately defined in physiological terms. They are usually accidents so that basic information such as the precise duration of a cardiac arrest or the blood pressure and heart rate during a period of severe hypotension is very rarely available. In such cases, neuropathological descriptions, however exhaustive, may well explain the final neuropsychiatric status of the patient but can at best indicate only tentatively the nature of the episode itself. The experimental approach is justified if it can indicate whether damage of a particular type in neurones and in white matter is or is not a direct consequence ofa particular hypoxic stress adequately delineated in physiological terms. At the outset it must be recalled that the energy for the normal functioning of the central nervous system is derived from the oxidative metabolism of glucose. A deficiency of oxygen or glucose will impair function and if severe and protracted enough will lead to irreversible brain damage. Interruption of the oxygen supply produces the most rapid impairment of brain function. Thus consciousness is lost about 10 sec after circulatory arrest. Abrupt anoxia exemplified by inhalation of an inert gas or sudden decompression to an altitude above 50 000 ft leads to loss of consciousnessafter aslightlylonger interval (17-20 sec). This rapid loss of consciousness in instances of profound hypoxia may well be responsible for the widely held view that enduring brain damage may begin soon after consciousness is lost.