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September 1987

Bilateral Basal Ganglia Necrosis Following Diffuse Hypoxic-lschemic Injury-Reply.

Author Affiliations

Department of Neurology University of Illinois at Chicago 912 S Wood St Chicago, IL 60612
Department of Neurology Tufts New England Medical Center Boston, MA 02111
Department of Ophthalmology University of Illinois at Chicago
Department of Neuro-ophthalmology Tufts New England Medical Center

Arch Neurol. 1987;44(9):897. doi:10.1001/archneur.1987.00520210005004

In Reply.  —We agree that the mechanism of bilateral pallidal necrosis as seen in hypoxic-ischemic brain injury is probably not related to anterior choroidal artery (AchA) compression, but rather metabolically mediated and due to selective vulnerability. Computed tomographic scans in our cases1 and those of Decroix et al2 of AchA infarcts always included involvement of the posterior limb of the internal capsule as do all necropsy cases.3-7 Furthermore, hypoxic ischemic injury also involves the thalamus and other structures distant from the AchA, and many patients have no evidence of brain swelling.

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