Artigo Revisado por pares

Afectación cortical inusual en un caso de encefalopatía de Wernicke

2006; Viguera Publishers; Volume: 42; Issue: 10 Linguagem: Inglês

10.33588/rn.4210.2005752

ISSN

1576-6578

Autores

O.J. Blanco Múñez, A. Suárez Gauthier, H. Martín García, V. Díaz Konrad, Victoria San Antonio Arce, Ana Cabello Fernández,

Tópico(s)

Alcoholism and Thiamine Deficiency

Resumo

Wernicke's encephalopathy (WE) is a metabolic disease due to thiamine deficiency; only 10% of cases are diagnosed pre-mortem. Symptoms of WE include ophthalmoplegia, nistagmus, ataxia and mental confusion; post-mortem examination shows characteristic symmetrical lesions in the mamillary bodies (MB), hypothalamus, thalamus, brain stem and cerebellum with spongiosis, demyelination, vascular proliferation and relative preservation of neurons.50 years-old male with alcoholic hepatopathy and orthotopic hepatic transplant who suffered a second surgical intervention 10 days after due to problems in the biliar anastomosis. After this second surgery he showed an altered mental status, with fluctuating global confusion, disorientation and agitation. He died 52 days after the hepatic transplantation. Autopsy study showed bilateral broncopneumonia, brown discoloration of the MB and bilateral linear lesions in the cortex of both motor gyri, which histologically showed identical to the MB lesions with demyelination, capillary and glial proliferation and preservation of neurons. Alzheimer type II astrocytes were also found in basal nuclei and cortex.Typical WE lesions affect MB, hypothalamus, thalamus, brain stem and cerebellum; cortical lesions, when found, are due to hepatocerebral degeneration with Alzheimer type II astrocytes or to the citopathic effects of ethanol. In our case, cortical lesions were identical to the lesions found in MB, an extraordinary finding which we have not found reported in the literature.

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