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Abstract • Three days after an episode of hypoxia, a 20-year-old man developed profound motor deficit in the absence of behavioral or cognitive disturbance. Previous reviews of delayed hypoxic encephalopathy have stressed behavioral and cognitive disturbances as the initial symptoms. This patient's pyramidal tract dysfunction in the absence of higher cortical dysfunction serves to illustrate that delayed hypoxic encephalopathy is predominantly a white matter rather than a gray matter disorder. References 1. Cramer A: Anatomischer Befund im Gehirn bei einer Kohlenoxydgasvergiftung . Zentrabl Allg Pathol 2:545-550, 1891. 2. Courville CB: The process of demyelination in the central nervous system . J Nerv Ment Dis 125:534-546, 1957.Crossref 3. Schwedenberg TH: Leukoencephalopathy following carbon monoxide asphyxia . J Neuropathol Exp Neurol 18:597-608, 1959.Crossref 4. Richardson JC, Chambers RA, Heywood PM: Encephalopathies of anoxia and hypoglycemia . Arch Neurol 1:178-190, 1959.Crossref 5. Plum F, Posner JB, Hain RF: Delayed neurological deterioration after anoxia . Arch Intern Med 110:56-63, 1962.Crossref 6. Brucher JM: Neuropathological problems posed by carbon monoxide poisoning and anoxia . Prog Brain Res 24:75-100, 1967. 7. Abbott CN, Courville CB: Degeneration of the globus pallidus after nitrous oxide anesthesia . Bull Los Angeles Neurol Soc 3:46-50, 1938. 8. Gebauer PW, Coleman FP: Postanesthetic encephalopathy following cyclopropane . Ann Surg 107:481-485, 1938.Crossref 9. Protass LM: Delayed postanoxic encephalopathy after heroin use . Ann Intern Med 74:738-739, 1971.Crossref 10. Bass NH: Pathogenesis of myelin lesions in experimental cyanide encephalopathy . Neurology 18:167-177, 1968.Crossref
Archives of Neurology – American Medical Association
Published: Oct 1, 1975
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