LAUSR

In “Miller Fisher syndrome and polyneuritis cranialis in COVID-19,” Gutiérrez-Ortiz et al. described 2 patients in Spain with COVID-19 and cranial nerve deficits: (1) a patient with Miller Fisher syndrome—anosmia, ageusia, and ophthalmoparesis—whose eye movements improved 2 weeks after treatment with intravenous immunoglobulin and (2) a patient with polyneuritis cranialis—manifested as bilateral abducens palsy—who recovered after conservative management. Vaira et al. hypothesized that, in patients with COVID-19, ageusia is likely because of direct viral effect on the ACE-2 receptors of taste buds and anosmia is likely the result of an inflammatory response. Vavougios further postulates that anosmia may be secondary to viral interaction with gangliosides on the olfactory nerves. Benito-Leόn et al. respond that the proposed mechanisms are certainly feasible but that the pathophysiology behind both cranial nerve deficits and other neurologic changes in patients with COVID-19 remains unclear. It is likely that COVID-19 affects the nervous system through a variety of different mechanisms. Further research is needed to identify the pathogenesis and treatment of cranial nerve deficits in patients with COVID-19. In particular, the editors wonder about the description of the ocular motility disturbance in case one as a right internuclear ophthalmoparesis and a right fascicular third nerve palsy. Typically, the lesions of Miller Fisher are extra-axial and may mimic palsies of central origin. In this case, the adduction palsy may have represented a pseudo-INO. Neuroimaging may have helped to distinguish the 2 possibilities.