RESUMO
Delayed anoxic encephalopathy after carbon monoxide (CO) poisoning is characterized by neurological deterioration that occurs after recovery from acute CO intoxication. There has been no established therapy. We report a patient recovered from acute CO intoxication developed various neurological symptoms. After the administration of high dose prednisolone and anticholinesterase inhibitor, the therapeutic effect was remarkable and confirmed by quantitative analysis of diffusion-tensor imaging (DTI). DTI could be used to evaluate the therapeutic effect for delayed anoxic encephalopathy after CO poisoning.
Assuntos
Humanos , Intoxicação por Monóxido de Carbono , Monóxido de Carbono , Carbono , Imagem de Tensor de Difusão , Hipóxia Encefálica , Leucoencefalopatias , Imageamento por Ressonância Magnética , Intoxicação , PrednisolonaRESUMO
A 53-year-old male patient presented with quadriparesis during pulmonological hospitalization for the treatment of S. aureus associated necrotizing pneumonia. He was diagnosed with the aquaporin-4 (AQP4) positive longitudinally extensive transverse myelitis from pons to T3 level. Despite the administration of intravenous methylprednisolone and plasma exchange with appropriate antibiotics, the patient's neurological condition deteriorated and he died. Our case implies that an S. aureus associated necrotizing pneumonia can trigger an AQP4 positive neuromyelitis optica spectrum disorder and contribute to the devastating course.