Shinichiro Ebihara

Effects of anoxia on cerebral metabolism and electrolytes in man

THE OXYGEN tension (PO,) of brain tissue obeys the law of supply and demand. Supply is influenced by arterial oxygen content, cerebral blood flow, and cerebral blood pH (by the Bohr effect), and demand depends soleIy on the functional state of brain metabolism. If the oxygen tension of the blood is reduced (for example, by anoxic anoxia of nitrogen inhalation), presumably a value will be reached below which capillary PO, is insufficient to maintain oxygen diffusion into brain tissue; functional impairment with signs of cerebral anoxia will result. Such thresholds for oxygen tension have been determined for brain preparations; below these cerebral oxygen consumption became decreased and thresholds for cerebral venous PO,-at which electroencephalographic slowing and decreased cerebral metabolism occurred-have also been estimated in animals by several investigators.1-5 There is as yet no comparable data available in man except a few determinations of the levels of oxygen saturation in the internal jugular vein at which loss of consciousness occurred during nitrogen breathing and postural hypotension.6 It has been reported in animals that when tissue or capillary venous pOz fell below threshold during induced anoxia the extracellular sodium ions of the brain decreased and there was an increase of extracellular potassium. This ionic change was said to correlate with electroencephalographic slowing.5,7rs Such data support the notion that anoxic symptoms and signs are due to failure of the mechanism for active sodium transport in brain, which is apparently dependent on cerebral energy metabolism. The present study reports for the first time in man similar observations concerning the threshold for cerebral venous oxygen tension

Creutzfeldt-Jakob disease: a case with extensive white matter degeneration and optic atrophy

SummaryA 52-year-old woman is described, whose clinical features were typical of Creutzfeldt-Jakob disease except for the presence of optic atrophy. Serial CT scans showed rapid development of brain atrophy early in the course. Postmortem examination revealed extensive degeneration of the cerebral and cerebellar white matter and of the optic nerves in addition to the classic findings of Creutzfeldt-Jakob disease. It is suggested that both the grey and white matter may undergo a severe destructive process early in the course of the disease, and the possibility is discussed that the white matter involvement is not a result of neuronal loss.ZusammenfassungDie klinischen Symptome einer 52 Jahre alten Frau mit typischer Creutzfeldt-Jakobscher Erkrankung und zusätzlich einer Atrophie des N. opticus werden beschrieben. Serienmäßige CT-Untersuchungen zeigten schon im Frünstadium der Erkrankung eine rasch fortschreitende Hirnatrophie. Autoptisch wurden neben den für die Creutzfeldt-Jakobsche Erkrankung klassischen Befunden eine ausgedehnte Degeneration der zerebralen und zerebellaren weißen Substanz sowie der Sehnerven gefunden. Diese Befunde deuten darauf hin, daß sowohl die graue als auch die weiße Substanz bereits im Frühstadium der Erkrankung schwer zerstört sein können und daß möglicherweise die Beteiligung der weißen Substanz nicht eine Folge neuronaler Schädigung ist.