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Delayed Postanoxic Encephalopathy After Strangulation Serial Neuroradiological and Neurochemical Studies
Ariyuki Hori, MD;
Genjiro Hirose, MD;
Satoshi Kataoka, MD;
Katsuyuki Tsukada, MD;
Kei Furui, MD;
Hisao Tonami, MD
Arch Neurol. 1991;48(8):871-874.
Abstract
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A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed lowdensity and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for -aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.
Author Affiliations
From the Departments of Neurology (Drs Hori, Hirose, Kataoka, Tsukada, and Furui) and Radiology (Dr Tonami), Kanazawa Medical University, Ishikawa, Japan.
Footnotes
Accepted for publication December 21, 1990.
Presented at the First International Stroke Congress, Kyoto, Japan, October 16,1989.
Reprint requests to Department of Neurology, Kanazawa Medical University, Uchinada, Kahoku, Ishikawa Prefecture, Japan 920-02 (Dr Hori).
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