Foncin J F, Le Beau J
Acta Neuropathol. 1978 Aug 7;43(1-2):153-9. doi: 10.1007/BF00685010.
A 24-year-old woman was found comatose after 2 days of cephalalgia and vomiting. An immediate diagnosis of carbon monoxyde poisoning was disclaimed when blood carbon monoxyde was found to be 1.75 ml/100. A diagnosis of acute intracranial hypertension led to trephination with ventricular punction and brain biopsy on the third day. The patient died on the eleventh day. Ultrastructural study of biopsy tissue showed nearly normal cortex, and injured white matter, with disrupted or destroyed myelin and pycnotic oligodendroglia in contrast with nearly normal axons, astrocytes, and capillaries. Autopsy showed a typical semioval center myelinopathy. After discussion of the histotoxic, vascular, and edema theories for myelinopathy pathogenesis, primary oligodendrogial lesion is considered, and correlated with the diphasic evolution often observed in the course of carbon monoxyde myelinopathy.
