RESUMEN
PURPOSE/AIM OF THE STUDY: A case admitted with dysarthria and syncope and hyperintense lesion in the splenium of the corpus callosum, diagnosed as Legionnaires' disease by detecting Legionella antigen in the urine, and recovered only with antibiotic treatment is presented because it is rare in the literature. MATERIALS AND METHODS: When a 64-year-old female patient was admitted to the emergency department with complaints of sudden loss of consciousness and fainting at home, she had speech impairment, and her pulse oxygen saturation in room air was 88%. In the neurological examination, there was no pathological finding except dysarthria in the patient with no motor deficit. The patient had no respiratory complaints and had a recent travel history. In laboratory examinations, hyponatremia was detected with increased C-reactive protein and liver enzymes. Consolidation was observed in the lower right zone on chest computed tomography. Ampicillin + sulbactam (4x1 gr, intravenous) and clarithromycin (2 × 500 mg orally) were initiated. On cranial magnetic resonance, a hyperintense lesion was observed in the splenium of the corpus callosum in the oval T2 sequence. Legionella pneumophila serogroup 1 antigen in urine was reported as positive. On the fourth day of her hospitalization, the patient, whose CRP and liver enzyme values regressed, her hyponatremia improved, her pulse oxygen saturation increased to 92% in room air, and her speech became comprehensible, was discharged after oral antibiotic treatment was arranged. On the 12th day, the speech ability of the patient completely returned to normal. CONCLUSION: Legionella infection should be suspected in the presence of pneumonia and corpus callosum splenium lesion.
RESUMEN
Clinically mild encephalitis/encephalopathy with a reversible splenial lesion is a clinicoradiological syndrome characterized by transient neuropsychiatric symptoms and hyperintensity of the splenium of the corpus callosum on diffusion-weighted MRI. Although intramyelinic edema and inflammatory cell infiltration can be predicted by MRI, the pathology of the splenium of the corpus callosum remains unknown. We encountered a case of clinically mild encephalitis/encephalopathy with a reversible splenial lesion and hypoglycemia in a patient who died of sepsis, and an autopsy was performed. The postmortem pathological findings included intramyelinic edema, myelin pallor, loss of fibrous astrocytes, microglial reactions, and minimal lymphocytic infiltration in the parenchyma. Based on these findings, transient demyelination following cytotoxic edema in the splenium of corpus callosum was strongly considered a pathogenesis of "clinically mild encephalitis/encephalopathy with a reversible splenial lesion" associated with hypoglycemia, and it could be generalized for the disease associated with the other causes. As cytotoxic edema could be the central pathology of the disease, the recently proposed term cytotoxic lesions of the corpus callosum may be applicable to this syndrome.