Parálisis ácida aguda "polio-like" (Brote de 10 casos presentados en Buenos Aires - Argentina en 2016) / Acute acid paralysis "polio-like" (Outbreak of 10 cases presented in Buenos Aires - Argentina in 2016)

RESUMEN

Resumen Objetivo Reportar un brote de 10 casos de mielopatías ácida aguda asimétrica por compromiso de la motoneurona espinal. Material y métodos: Relación V/M 6/4 media de edad de 3 años, todos con parálisis ácida aguda, analizamos sus aspectos clínicos, etiológicos, neurorradiológicos, terapéuticos y evolutivos. Resultados: 8 presentaron parálisis áccida de miembros superiores asimétrica, 1 monoplejía de miembro inferior izquierdo, 1 hemiparesia, 5 sumaron compromiso de pares craneanos y 4 requirieron asistencia respiratoria mecánica. Todos coincidieron con catarro de vía aérea superior y/o ebre. La resonancia magnética medular fue anormal en todos, identi cando dos patrones de imágenes uno lineal relacionado al compromiso del asta anterior y otro más heterogéneo con médula espinal engrosada, sin refuerzo con contraste, 5/10 presentaron además compromiso bulbo-protuberancial. Ninguno presento lesiones supratentoriales. En 4/10 identi camos enterovirus humano subtipo D68 HEV-D68) en secreciones de vía aérea y en 1/10 de ellos también en LCR. En el resto se detectaron otros enterovirus A, B y C, en uno rinovirus y otro In uenza. Nueve pacientes recibieron como tratamiento gammaglobulina y corticoides y 4 además recambio plasmático terapéutico sin mejoría clínica. Conclusiones: Ante una parálisis ácida aguda es importante descartar el HEV-D68. Consideramos los casos no detectados como "falsos negativos" dado que las muestras fueron tomadas tardíamente. Los otros virus identi cados no se han relacionado a mielopatías. Si bien la siopatología no es clara la ausencia de respuesta a tratamiento antin amatorio e inmunomodulador orienta a un mecanismo de agresión directa del virus. Se trata del primer reporte por HEV-D68 en Latinoamérica.

ABSTRACT

Abstract Objective: To report an outbreak of 10 cases of acute asymmetric accid myelopathy due to spinal motor neuron injury. Material and methods: Ten children, six male, with a mean age of 3 years presented with acute accid myelitis. We analyzed clinical features, etiology, neuroradiological images, treatment, and outcome. Results: Eight children had bilateral and asymmetric accid myelitis of the upper limbs, 1 had upper limb monoplegia, and 1 presented with hemiparesis. The cranial nerves were involved in 5 patients and 4 required mechanical ventilation. In all cases acute accid myelitis co-occurred with upper airway infection and/or fever. Spinal cord magnetic resonance imaging was abnormal in all, showing 2 di erent patterns A linear pattern involving the anterior horns and another that was more heterogeneous showing spinal cord expansion. The lesions were non-enhancing in all. In 5/10 patients involvement of the medulla oblongata and pons was also observed. None of the patients presented with supratentorial lesions. In 4/10 children, the human enterovirus subtype D68 (HEV-D68) was identi ed in the airway and in 1/10 in the cerebrospinal uid as well. In the remaining patients di erent enterovirus species A, B, and C variants were detected, as well as rhinovirus in 1 and in uenza in another. Nine children received treatment with intravenous immunoglobulin and steroids and 4 of these children also underwent plasma exchange. Treatment did not lead to clinical improvement. Conclusions: In a patient with acute accid myelitis, HEV-D68 infection should be ruled out. Cases in which the virus was not detected were considered as "false negatives" as samples were collected late in course of the disease. The lack of response to anti-in ammatory and immunomodulatory treatment suggests a direct viral mechanism. This study is to our knowledge the rst on an HEV-D68-infection-related report in Latin America.