Mild Encephalopathy/Encephalitis With a Reversible Splenial Lesion (MERS) and Longitudinally Extensive Transverse Myelitis (LETM) in Influenza B: Neurotropic Mechanisms and Diagnostic Challenges

Abstract

Mild encephalopathy/encephalitis with a reversible splenial lesion (MERS) and longitudinally extensive transverse myelitis (LETM) are neuroinflammatory conditions related to the brain and spinal cord, respectively. Most cases of MERS and LETM are related to a secondary autoimmune process in response to an initial insult (i.e., infection, immunization, etc.). The case of an 18-year-old female who developed a three-day history of fever, quadriplegia, cough, and mild encephalopathy is reported here. The patient tested positive for influenza B by nasopharyngeal swab with polymerase chain reaction (PCR). Initial magnetic resonance imaging (MRI) revealed the presence of a diffusion-restricted non-enhancing lesion confined to the splenium of the corpus callosum (MERS type I) and longitudinally extensive non-enhancing T2 hyperintensities from C1 to C5. The patient was managed with a five-day course of 1,000 mg of intravenous methylprednisolone (IVMP). Additionally, five days of therapeutic plasmapheresis (PLEX) was completed. The patient showed significant improvement with medical management and physical therapy. At the one-year follow-up, her motor symptoms had resolved and endorsed only mild paresthesia in the upper extremities. A repeat MRI revealed a reversal of the splenium lesion and moderate improvement in T2 hyperintensities of the cervical cord. Assessing neuroinvasion of the influenza virus is difficult, and diagnostic challenges arise in determining primary infectious versus autoimmune-mediated neuroinflammation. A review of the literature on influenza infection with radiographic findings of MERS and LETM is included.

Keywords: corpus callosum; encephalomyelitis; infectious encephalitis; influenza b; influenza virus; longitudinally extensive transverse myelitis; mild encephalopathy/encephalitis with reversible splenial lesion; neuroinfectious diseases; neurotropism; splenium.

Figure 1. MRI of the brain and cervical spinal cord

(A) T2 FLAIR sagittal sequence shows a non-enhancing lesion in the splenium of the corpus callosum (arrows). (B) T2 FLAIR sagittal sequence of the cervical spinal cord with hyperintensities from C1 to C5 (arrows). (C) DWI sequence depicts diffusion restriction within the splenium of the corpus callosum (arrow). (D) ADC sequence confirming the aforementioned diffusion restriction (arrow). (E and F) T1-weighted imaging with only mild hypointensity in the splenium of the corpus callosum (arrow) and without enhancement. MRI: magnetic resonance imaging, FLAIR: fluid-attenuated inversion recovery, DWI: diffusion-weighted imaging, ADC: apparent diffusion coefficient

Figure 2. MRI (axial view) of the cervical spine

(A-D) T2 FLAIR (axial view) of spinal segments C2-C5 reveals primarily gray matter hyperintensities (arrows). MRI: magnetic resonance imaging, FLAIR: fluid-attenuated inversion recovery

Figure 3. Repeat MRI of the brain and cervical spine

(A) MRI of the brain T2/FLAIR sagittal sequence reveals resolution of previous splenium lesion on the corpus callosum. (B) MRI of the cervical spine T2/FLAIR sagittal sequence depicts improvement in hyperintense lesions (arrow). MRI: magnetic resonance imaging, FLAIR: fluid-attenuated inversion recovery

Figure 4. Proposed mechanisms of viral neurotropism

Image credits: Bahadar S. Srichawla

Figure 5. Proposed mechanisms of viral autoimmunity

Image credits: Bahadar S. Srichawla