Abstract

Corpus callosum includes a large amount of axons with various degrees of myelination, interconnecting cerebral hemispheres. Tumors, demyelinating diseases, infections, trauma and metabolic diseases as well as vascular lesions may affect corpus callosum, often extending to other white matter areas of the brain. We describe the case of a 76 years old male patient with history of arterial hypertension, diabetes mellitus and normal pressure hydrocephalus, developing dysphagia during hospitalization. Ab-ingestis pneumonia caused brain hypoxia and coma; brain magnetic resonance disclosed isolated demyelination of corpus callosum that was not present before hypoxia. Compared to neurons and astrocytes, oligodendrocytes are reported as particularly sensitive to hypoxia. Respiratory involvement without blood flow impairment could have lead to a prevalent oligodendrocytes damage, resulting in a selective demyelination of corpus callosum. Our patient indeed evolved into persistent vegetative state and died five months after hypoxic episode. This case report could give some insight about in vivo brain susceptibility to hypoxic damage.

Highlights

  • Corpus callosum (CC) is the most important cerebral inter-hemispheric connecting structure, characterized by densely packed myelinated and unmyelinated white matter tracts originating by cortical neurons

  • We describe a patient developing isolated CC lesions following hypoxic damage, with consequent coma, vegetative state and death

  • We describe a patient developing isolated demyelination of CC following brain hypoxia due to ab-ingestis pneumonia

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Summary

Isolated Demyelination of Corpus Callosum Following Hypoxia

Corpus callosum includes a large amount of axons with various degrees of myelination, interconnecting cerebral hemispheres. Tumors, demyelinating diseases, infections, trauma and metabolic diseases as well as vascular lesions may affect corpus callosum, often extending to other white matter areas of the brain. We describe the case of a 76 years old male patient with history of arterial hypertension, diabetes mellitus and normal pressure hydrocephalus, developing dysphagia during hospitalization. Compared to neurons and astrocytes, oligodendrocytes are reported as sensitive to hypoxia. Respiratory involvement without blood flow impairment could have lead to a prevalent oligodendrocytes damage, resulting in a selective demyelination of corpus callosum. Our patient evolved into persistent vegetative state and died five months after hypoxic episode. This case report could give some insight about in vivo brain susceptibility to hypoxic damage

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