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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia.

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys.Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.[1]


  1. Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia. Harber, E.S., O'Sullivan, M.G., Jayo, M.J., Carlson, C.S. Vet. Pathol. (1996) [Pubmed]
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