MR imaging findings of enteroviral encephaloymelitis: an outbreak in Taiwan

Abstract

Background and purpose: An outbreak of enterovirus infection occurred in Taiwan from late spring to early fall of 1998. Most of the pediatric infections presented as hand-foot-mouth disease (HFMD) and herpangina. A small portion of patients had symptoms of polio-like encephalitis and paralysis. The purpose of this study was to review the MR imaging findings in CNS involvement of enterovirus infection.

Methods: Twenty patients who had HFMD and clinical encephalitis were examined with MR imaging. T1-weighted and T2-weighted MR images were obtained. From the rectum, throat, CSF, and peripheral blood, the presence of enterovirus 71 (EV 71) was determined by virus culture, immunofluorescent microscopy, immunologic dot blotting, and reverse-transcription polymerase chain reaction.

Results: MR imaging studies of 20 patients showed hyperintensity in the brain stem and spinal cord in 15 patients, as seen on T2-weighted images. The major CNS lesions were in the medulla oblongata, pons, midbrain, and the dentate nuclei of the cerebellum. In some cases, the lesions involved the spinal cord (three cases) as well as the thalamus (two cases) and putamina (one case). Five patients had normal MR imaging results. After the appropriate management for tachycardia and tachypnea, 18 patients recovered within 1 to 2 weeks. In the follow-up MR imaging examination of five patients, the lesions completely disappeared within 2 weeks to 2 months. In two patients who were still respirator-dependent, MR imaging showed the tissue destruction in the posterior portions of the medulla, pons, and the ventral horns of cervical spinal cord. In one patient, most of midbrain was damaged. The presence of EV 71 was detected in specimens from 18 patients.

Conclusion: Because EV 71 was identified in 18 patients, and no other virus was detected, EV 71 was determined to be the major causative agent of this encephalomyelitis. Brain stem and cervical spinal cord involvement are characteristic findings of enteroviral encephalomyelitis.

Figures

fig 1.

Male patient, 4 years old. Acute EV 71 encephalitis. Patient presented with HFMD on June 10, 1998. Two days later, patient developed somnolence, tachycardia, and tachypnea. All MR images are T2-weighted images (3567/120/6 [TR/TE/excitations]). A, Hyperintense lesions in the posterior portion of the medulla oblongata (arrow) and the bilateral dentate nuclei (arrowheads) of the cerebellum. B, Hyperintense lesions in the posterior portion of the pons (arrow). C, Hyperintense lesions in central-most portion of the midbrain (arrows). D–F, Patient completely recovered without any sequelae. Follow-up MR imaging on July 29, 1998. The hyperintense lesions in the medulla, pons, midbrain, and dentate nuclei had disappeared. (The mild high-signal intensity of the posterior portion of the pons is normal in infants, possibly because of its under-myelinated status.)

fig 2.

Female patient, 10 months old. Chronic stage of EV 71 encephalomyelitis. Patient presented with HFMD on June 20, 1998. Two days later, patient developed somnolence, tachycardia, tachypnea, and coma. Patient recovered very slowly, awaking in September. Patient remained ventilator- and oxygen-dependent. MR imaging was performed on September 22, 1998. All images are T2-weighted images (3560/120/6 [TR/TE/excitations]). A, In sagittal sections, the lesions appear as a linear high signal in the posterior portions of the pons and medulla oblongata (arrows) and in the whole cervical spinal cord (white arrows). B, Two symmetrical, well-defined hyperintense lesions in the cervical spinal cord (arrows), corresponding to the locations of ventral horns of the spinal cord.

fig 3.

C (T1-weighted image) and D (T2-weighted image), Discrete lesions also were seen in the posterior aspect of the pons (arrows) and dentate nuclei (arrowheads). The nuclei of V, VI, VII, IX nerves were destroyed. E and F (T1-weighted images), Most of the midbrain was destroyed, including the red nuclei, substantia nuclei, the medial lemniscus, and the nuclei of III and IV nerves. G (T1-weighted image), Lesions are noted in the bilateral thalami (short arrows) and the putamina (long arrows). H (T1-weighted image), Two symmetrical lesions within the cervical spinal cord (arrows), corresponding to the locations of the ventral horns. Female patient, 22 months old. Chronic stage of EV 71 encephalomyelitis. Patient presented with HFMD on July 17, 1998. Two days later, she developed a sudden consciousness change, tachycardia, tachypnea, then coma. MR imaging was performed on October 16, 1998, while the patient was in a vegetative state and respirator-dependent. T2-weighted images (3567/120/4 [TR/TE/exciations]) and T1-weighted images (553/20/2) were performed. A and B, Very low-signal intensity lesions on T1-weighted image (A) and bright on T2-weighted image (B) in the posterior portion of the medulla oblongata (arrows). The dorsal nucleus of the vagus nerve, the nuclei of the solitary tract, and the medial longitudinal fasciculus were destroyed. There were fluid accumulations in the bilateral mastoids, reflecting mastoiditis.