Delayed postanoxic encephalopathy after strangulation. Serial neuroradiological and neurochemical studies
A. Hori, G. Hirose, S. Kataoka, K. Tsukada, K. Furui and H. Tonami
Department of Neurology, Kanazawa Medical University, Ishikawa, Japan.
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 low-density 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 gamma-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.
