A Post-Infectious Steroid-Responsive Brainstem Lesion Associated With COVID-19

Abstract

A 51-year-old man developed coma, bilateral pupillary dilation, ophthalmoplegia and quadriplegia 4 weeks after testing positive for COVID-19. MRI demonstrated a symmetric midline pontine non-enhancing T2-FLAIR hyperintense lesion. The patient was treated with intravenous methylprednisolone, which resulted in improvement of his Glasgow Coma Scale (GCS) from 3 to 15 over the next 5 days. To our knowledge, this is the first case of a post-infectious steroid-responsive brainstem lesion associated with COVID-19. The clinical picture best fits in the family of a steroid-responsive encephalopathy and reminds us that COVID-19 may cause severe post-infectious neurological complications.

An overview of third, fourth and sixth cranial nerve palsies in the setting of COVID-19: A case report and systematic review

“…[ 4 , 8 , 12 , 18 , 24 , 26 ] Corticosteroids were used in the management of other cases. [ 2 , 20 , 30 , 31 ]…”

“…Whether there is a predilection for SARS-CoV-2 infection of the Abducent nerve compared to other oculomotor nerves remains a question to be answered. Some patients experienced ophthalmoplegia due to stroke through affection of the occipital lobe, brainstem [29,30] or right branch retinal occlusion. [22] The pathology was detected by MRI in most cases while it was unclear in others.. [20,24,28,31] In our case, MRI was normal as in (Fig.…”

Anti-neuronal antibodies against brainstem antigens are associated with COVID-19

“… 4 Brainstem injury in COVID-19 is now documented with a variety of clinical manifestations including disorders of eye-movements, coordination, consciousness, as well as involuntary movements. 5 , 6 Concomitant imaging findings range from normal, through isolated lesions, to extensive tissue loss and have been described as brainstem encephalitis, rhombencephalitis, or acute necrotising encephalopathy. 5 , 6 , 7 , 8 …”

“… 5 , 6 Concomitant imaging findings range from normal, through isolated lesions, to extensive tissue loss and have been described as brainstem encephalitis, rhombencephalitis, or acute necrotising encephalopathy. 5 , 6 , 7 , 8 …”

“…First, immunomodulation is usually at least partially effective. 5 , 6 , 7 , 8 , 11 , 12 Second, cerebrospinal fluid (CSF) from patients with neurological manifestations contains high pro-inflammatory cytokine levels. 13 Third, CSF-immunohystochemistry shows brainstem-binding antibodies (Abs).…”