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January 1976

Hypoxic-Ischemic Leukoencephalopathy in Man

Author Affiliations

From the Charles S. Kubik Laboratory for Neuropathology of the James Homer Wright Pathology Laboratories, Massachusetts General Hospital, Boston (Drs Ginsberg and Richardson), the Department of Pathology, Beth Israel Hospital, Boston (Dr Hedley-Whyte), and the Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia (Dr Ginsberg); and the departments of neurology and neuropathology, Harvard Medical School, Boston; and the Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia.

Arch Neurol. 1976;33(1):5-14. doi:10.1001/archneur.1976.00500010007002

• Three cases of hypoxic-ischemic leukoencephalopathy were studied. In two patients, the neurologic disorder followed drug overdosage; in the third, the apparent precipitating event was a postoperative myocardial infarction complicated by circulatory insufficiency. All patients were deeply unresponsive, with varying reflex patterns. In all three cases, the brain showed extensive symmetrical necrotic lesions of the central white matter, with minimal damage to gray matter structures. The lesions in case 3 showed, in addition, vascular necrosis and ring hemorrhages. Common to all cases was a prolonged period of hypoxemia, hypotension, and elevated venous pressure. Acidosis occurred in two. These observations and analysis of previous reports of similar cases suggest that leukoencephalopathy tends to occur when the hypoxemia is prolonged and is associated with periods of hypotension and metabolic imbalance.

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