Reader response: Miller Fisher Syndrome and polyneuritis cranialis in COVID-19
Luigi AngeloVaira, Maxillofacial Surgeon, University Hospital of Sassari
GiovanniSalzano, Maxillofacial Surgeon, University of Naples "Federico II" Hospital
GiacomoDe Riu, Maxillofacial Surgeon, University Hospital of Sassari
Submitted April 28, 2020
We read with interest the report by Gutiérrez-Ortiz et al.1 Starting from the analysis of two cases of Miller Fisher Syndrome and cranial polyneuritis, the authors propose some hypotheses regarding the pathogenesis of neurologic manifestations during COVID-19. They affirm that there may be a common pathogenesis among all neurologic clinical features of COVID-19, including chemosensitive disorders, which appear frequently in these patients in Europe.
In recent weeks, we have gained a great deal of experience with these types of dysfunctions, which appear to affect more than 70% of COVID-19 cases.2,3 Based on the clinical evaluation of these patients, we also asked ourselves what the pathogenesis of these disorders could be.4 Anosmia and ageusia during COVID-19 generally regress within 1–2 weeks. Moreover, their frequency seems to be much higher than any manifestation linked to a central nervous system involvement. For these reasons, neurologic manifestations are more likely to be linked to inflammatory phenomena than to invasion of the central nervous system with neuronal damage. Specifically, as regards anosmia, the target of the virus could be represented by non-neuronal supporting cells of the olfactory epithelium and pathway, which negatively influence the activity of olfactory neurons through inflammatory mechanisms.5
The alteration of the gustatory function—which has a greater tendency to resolve than olfaction—could instead be altered by the direct action of the virus on the ACE-2 receptors of the taste buds. Besides, ageusia is a well-known side effect of ACE-2 inhibitors.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Gutiérrez-Ortiz C, Méndez A, Rodrigo-Rey S, et al. Miller Fisher Syndrome and polyneuritis cranialis in COVID-19. Neurology 2020 Epub Apr 17.
Vaira LA, Salzano G, Deiana G, De Riu G. Anosmia and ageusia: common findings in COVID-19 patients. Laryngoscope 2020 Epub Apr 1.
Vaira LA, Deiana G, Fois AG et al. Objective Evaluation of Anosmia and Ageusia in COVID-19 Patients: Single-center Experience on 72 Cases. Head Neck 2020 Epub Apr 27.
Vaira LA, Salzano G, Fois AG, Piombino P, De Riu G. Potential pathogenesis of ageusia and anosmia in COVID-19 patients. Int Forum Allergy Rhinol 2020 Epub Apr 27.
Brann DH, Tsukahara T, Weinreb C et al. Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia. BioRxiv 2020 Epub Apr 9. Available at: https://www.biorxiv.org/content/10.1101/2020.03.25.009084v3.
We read with interest the report by Gutiérrez-Ortiz et al.1 Starting from the analysis of two cases of Miller Fisher Syndrome and cranial polyneuritis, the authors propose some hypotheses regarding the pathogenesis of neurologic manifestations during COVID-19. They affirm that there may be a common pathogenesis among all neurologic clinical features of COVID-19, including chemosensitive disorders, which appear frequently in these patients in Europe.
In recent weeks, we have gained a great deal of experience with these types of dysfunctions, which appear to affect more than 70% of COVID-19 cases.2,3 Based on the clinical evaluation of these patients, we also asked ourselves what the pathogenesis of these disorders could be.4 Anosmia and ageusia during COVID-19 generally regress within 1–2 weeks. Moreover, their frequency seems to be much higher than any manifestation linked to a central nervous system involvement. For these reasons, neurologic manifestations are more likely to be linked to inflammatory phenomena than to invasion of the central nervous system with neuronal damage. Specifically, as regards anosmia, the target of the virus could be represented by non-neuronal supporting cells of the olfactory epithelium and pathway, which negatively influence the activity of olfactory neurons through inflammatory mechanisms.5
The alteration of the gustatory function—which has a greater tendency to resolve than olfaction—could instead be altered by the direct action of the virus on the ACE-2 receptors of the taste buds. Besides, ageusia is a well-known side effect of ACE-2 inhibitors.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References