Summary
We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to refect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.
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References
Brierley JB, Graham DI (1984) Hypoxia and vascular disorders of the central nervous system. In: Adams JH, Corsellis JAN, Duchen LW (eds) Greenfield's neuropathology, 4th edn. Arnold, London, pp 125–207
Neubuerger KT (1954) Lesions of the human brain following circulatory arrest. J Neuropathol Exp Neurol 13: 144–160
Ginsberg MD, Hedley-Whyte ET, Richardson EP (1976) Hypoxic-Ischemic leukoencephalopathy in man. Arch neurol 33: 5–14
Yagnik P, Gonzalez C (1980) White matter involvement in anoxic encephalopathy in adults. J Comput Assist Tomogr 4: 788–790
Liwnicz BH, Mouradian MD, Ball Jr JB (1987) Intense brain cortical enhancement on CT in laminar necrosis verified by biopsy. AJNR 8: 157–159
Kjos BO, Brant-Zawadzki M, Young RG (1983) Early CT findings of global central nervous system hypoperfusion. Am J Radiol 141: 1227–1232
Richardson ML, Kinard RE, Gray MB (1981) CT of generalized gray matter infarction due to hypoglycemia. AJNR 2: 366–367
Mitchell MR, Smith GD (1988) MRI tissue characterization: In: Partain CL, Price RR, Patton JA, Kulkarni MV, James Jr AE (eds) Magnetic resonance imaging, 2nd edn. Sanders, Philadelphia, pp 87–89
Lumsden CE (1970) Pathogenetic mechanisms in the leucoencephalopathies in anoxic-ischaemic processes, in disorders of the blood and in intoxications. In: Vinken PJ, Bruyn GW (eds) Handbook of clinical neurology, vol 9. North-Holland publishing, Amsterdam, American Elsevier publishing, New York, pp 572–663
Okeda R, Funata N, Takano T, Miyazaki Y, Higashino F, Yokoyama K, Manabe M (1981) The pathogenesis of carbon monoxide encephalopathy in the acute phase physiological and morphological correlation. Acta Neuropathol (Berl) 54: 1–10
Ginsberg MD, Myers RE (1974) Experimental carbon monoxide encephalopathy in the primate. Arch Neurol 30: 202–208
Salama J, Gherardi R, Amiel H, Poirier J, Delaporte P, Gray F (1986) Post-anoxic delayed encephalopathy with leukoencephalopathy and non-hemorrhagic cerebral amyloid angiopathy. Clin Neuropathol 5: 153–156
Zulch KJ (1981) The cerebral infarct. Pathology, pathogenesis, and computed tomography. Springer, Berlin Heidelberg New York Tokyo, pp 1–20
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Sawada, H., Udaka, F., Seriu, N. et al. MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy. Neuroradiology 32, 319–321 (1990). https://doi.org/10.1007/BF00593053
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DOI: https://doi.org/10.1007/BF00593053