Objectives: To review our current knowledge of the etiopathogenesis of Bell's palsy, including viral infection or autoimmunity, and to discuss disease pathogenesis with respect to pharmacotherapy. Systematic review methodology: Relevant publications on the etiopathogenesis, clinical presentation, diagnosis and histopathology of Bell's palsy from 1975 to 2012 were analysed. Results and conclusions: Bell's palsy is an idiopathic peripheral nerve palsy involving the facial nerve. It accounts for 60 to 75% of all cases of unilateral facial paralysis. The annual incidence of Bell's palsy is 15 to 30 per 100,000 people. The peak incidence occurs between the second and fourth decades (15 to 45 years). The aetiology of Bell's palsy is unknown but viral infection or autoimmune disease has been postulated as possible pathomechanisms. Bell's palsy may be caused when latent herpes viruses (herpes simplex, herpes zoster) are reactivated from cranial nerve ganglia. A cell-mediated autoimmune mechanism against a myelin basic protein has been suggested for the pathogenesis of Bell's palsy. Bell's palsy may be an autoimmune demyelinating cranial neuritis, and in most cases, it is a mononeuritic variant of Guillain-Barre syndrome, a neurologic disorder with recognised cell-mediated immunity against peripheral nerve myelin antigens. In Bell's palsy and CBS, a viral infection or the reactivation of a latent virus may provoke an autoimmune reaction against peripheral nerve myelin components, leading to the demyelination of cranial nerves, especially the facial nerve. Given the safety profile of acyclovir, valacyclovir, and short-course oral corticosteroids, patients who present within three days of the onset of symptoms should be offered combination therapy. However it seems logical that in fact, steroids exert their beneficial effect via immunosuppressive action, as is the case in some other autoimmune disorders. It is to be hoped that (monoclonal) antibodies and/or T-cell immunotherapy might provide more specific treatment guidelines in the management of Bell's palsy. (C) 2012 Elsevier B.V. All rights reserved.

Bell's palsy and autoimmunity / Greco, Antonio; Gallo, Andrea; Fusconi, Massimo; Marinelli, Caterina; Macri, GIAN FRANCO; DE VINCENTIIS, Marco. - In: AUTOIMMUNITY REVIEWS. - ISSN 1568-9972. - STAMPA. - 12:2(2012), pp. 323-328. [10.1016/j.autrev.2012.05.008]

Bell's palsy and autoimmunity

GRECO, Antonio;GALLO, Andrea;FUSCONI, Massimo;MARINELLI, CATERINA;MACRI, GIAN FRANCO;DE VINCENTIIS, Marco
2012

Abstract

Objectives: To review our current knowledge of the etiopathogenesis of Bell's palsy, including viral infection or autoimmunity, and to discuss disease pathogenesis with respect to pharmacotherapy. Systematic review methodology: Relevant publications on the etiopathogenesis, clinical presentation, diagnosis and histopathology of Bell's palsy from 1975 to 2012 were analysed. Results and conclusions: Bell's palsy is an idiopathic peripheral nerve palsy involving the facial nerve. It accounts for 60 to 75% of all cases of unilateral facial paralysis. The annual incidence of Bell's palsy is 15 to 30 per 100,000 people. The peak incidence occurs between the second and fourth decades (15 to 45 years). The aetiology of Bell's palsy is unknown but viral infection or autoimmune disease has been postulated as possible pathomechanisms. Bell's palsy may be caused when latent herpes viruses (herpes simplex, herpes zoster) are reactivated from cranial nerve ganglia. A cell-mediated autoimmune mechanism against a myelin basic protein has been suggested for the pathogenesis of Bell's palsy. Bell's palsy may be an autoimmune demyelinating cranial neuritis, and in most cases, it is a mononeuritic variant of Guillain-Barre syndrome, a neurologic disorder with recognised cell-mediated immunity against peripheral nerve myelin antigens. In Bell's palsy and CBS, a viral infection or the reactivation of a latent virus may provoke an autoimmune reaction against peripheral nerve myelin components, leading to the demyelination of cranial nerves, especially the facial nerve. Given the safety profile of acyclovir, valacyclovir, and short-course oral corticosteroids, patients who present within three days of the onset of symptoms should be offered combination therapy. However it seems logical that in fact, steroids exert their beneficial effect via immunosuppressive action, as is the case in some other autoimmune disorders. It is to be hoped that (monoclonal) antibodies and/or T-cell immunotherapy might provide more specific treatment guidelines in the management of Bell's palsy. (C) 2012 Elsevier B.V. All rights reserved.
2012
aetiology; pathogenesis; bell's palsy; therapy; autoimmunity
01 Pubblicazione su rivista::01a Articolo in rivista
Bell's palsy and autoimmunity / Greco, Antonio; Gallo, Andrea; Fusconi, Massimo; Marinelli, Caterina; Macri, GIAN FRANCO; DE VINCENTIIS, Marco. - In: AUTOIMMUNITY REVIEWS. - ISSN 1568-9972. - STAMPA. - 12:2(2012), pp. 323-328. [10.1016/j.autrev.2012.05.008]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/463596
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