COVID-19 LEUKOENCEPHALOPATHY: THE MIDDLE CEREBELLAR PEDUNCLE SIGN

Abstract

TOPIC: Imaging TYPE: Medical Student/Resident Case Reports INTRODUCTION: Although the pulmonary manifestations of the coronavirus disease 2019 (COVID-19) are commonly recognized, a rapidly accumulating body of evidence also supports multiple neurological manifestations. In addition to nonspecific headache and myalgia, complications include cranial/peripheral neuropathy, meningoencephalitis, and acute demyelination. We now present a case of acute encephalomyelitis associated with COVID-19. CASE PRESENTATION: A 69-year-old male with a history of diabetes mellitus and was admitted to the intensive care unit. He initially presented to the emergency room four days prior for fevers at which time COVID-19 PCR rapid antigen testing was positive. He was discharged home given the absence of other symptoms. Four days later he was found unresponsive and intubated for airway protection. On arrival to the hospital, the patient was unresponsive with roving eye movements but withdrew to stimulation in all extremities. He was started on dexamethasone and remdesivir. Computed tomography head demonstrated mild chronic small vessel ischemic periventricular leukomalacia. Given the degree of his encephalopathy, an magnetic resonance imaging (MRI) T2 of the brain was obtained demonstrating bilaterally symmetric restricted diffusion at the middle cerebellar peduncles and corticospinal tracts without microbleeds (Figure 1). FLAIR hyperintense lesions in the dorsal aspects of the internal capsules extending into the corticospinal tracts at the midbrain were also noted. A lumbar puncture was remarkable for 100% lymphocytic predominance cell count with normal glucose and protein. Steroid therapy was transitioned to methylprednisolone 1 gram daily for 5 days. Although repeat MRI (Figure 2) one week later showed lessened restriction diffusion without new pathology, the patient remained profoundly encephalopathic. Given the stability on MRI, intravenous immunoglobulin was deferred. He was started on a prednisone taper. He subsequently had a tracheostomy and percutaneous gastrostomy tube placed and transferred to a long-term acute care hospital. DISCUSSION: This case highlights an important finding of middle cerebellar peduncle lesions on MRI in the setting of COVID-19. Neurologic symptoms from COVID-19 are becoming better understood, with multiple recent papers examining neurological sequelae. The mechanism by which COVID-19 causes demyelination is not entirely clear. One idea is that leukocytes that become infected can serve as a reservoir and a vector of the disease that are subsequently able to enter the CNS through the bloodstream. Another theory is that viruses will infect peripheral neurons and then using axonal transport machinery will access the central nervous system. CONCLUSIONS: More research needs to be done to identify a precise mechanism of how demyelination occurs, but it is clear that demyelination is an unfortunate outcome of infection with respiratory viruses, like COVID-19. REFERENCE #1: Kremer S et al (Neurology 2020; 95: e1868-e1882) reported radiographic ADEM with COVID-19; MCP involvement reported as well as meningeal enhancement. REFERENCE #2: Desforges M, Coupanec AL, Dubeau P, et al. Human Coronaviruses and Other Respiratory Viruses: Underestimated Opportunistic Pathogens of the Central Nervous System? Viruses. 2019, 12, 14. DISCLOSURES: No relevant relationships by HANAD BASHIR, source=Web Response No relevant relationships by Mark Metry, source=Web Response No relevant relationships by Aidan Neustadtl, source=Web Response No relevant relationships by Christopher Newey, source=Web Response