RESUMEN
Wernicke's encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine deficiency. Traditionally, diagnosis of WE rests on a clinical symptom triad consisting of ocular signs, altered consciousness, and ataxia. However, the complete triad is only present in a fraction of cases, which means that WE tends to be under-diagnosed, especially in nonalcoholic patients. Brain MRI of WE patients usually shows symmetrical signal intensity alterations in the thalami, mammillary bodies, and periaqueductal area, because of cytotoxic edema in the same region. These typical findings are useful diagnostic leads in WE patients with atypical symptoms. However, atypical findings can occasionally be seen in the vermis of cerebellum and cerebellar nuclei. Notably, alterations of signal intensity in the cerebellar dentate nuclei, which is a typical finding of metronidazole-induced encephalopathy (MIE), need to be distinguished according to medication history and response to thiamine.
Asunto(s)
Humanos , Ataxia , Encéfalo , Núcleos Cerebelosos , Cerebelo , Estado de Conciencia , Edema , Tubérculos Mamilares , Metronidazol , Tiamina , Deficiencia de Tiamina , Encefalopatía de WernickeRESUMEN
Spontaneous renal artery dissection without aortic dissection in normotensive patients is rarely reported. Spontaneous renal artery dissection is also an uncommon cause of renal infarction that occurs, though rarely, in patients with hypercoagulable states such as protein C and S deficiency. We report here a case of spontaneous renal artery dissection and renal infarction associated with protein C and S deficiency.