Bell's Palsy: A Need for Paradigm Shift?

Abstract

Introduction Bell's palsy (BP) is considered to be idiopathic facial palsy. Some schools of thought believe it to be a part of polyneuropathy, whereas other scientists have other plausible explanations for the condition and all these were reviewed. Methods The literature on BP was retrieved using the Cochrane Database of Systematic Reviews, PubMed, and Google Scholar. Keywords and phrases used during the search included “Bell's palsy,” “polyneuropathy,” “anatomical factors,” and “autoimmunity.” Results There are only few studies that have tried to find out the association of BP with peripheral nerve conduction abnormalities. In most studies conducted, positive correlation was found. There are many theories of its etiology, with the reactivation of herpes simplex virus isoform 1 and/or herpes zoster virus (HZV) from the geniculate ganglia being the most strongly suspected cause. Conclusion In the future, large studies will be required to determine the association between peripheral neuropathy and BP and elucidate the real etiology in every case. There will also be a need to determine whether BP should still be considered idiopathic and isolated.

Computed tomographic features of the proximal petrous facial nerve canal in recurrent Bell's palsy

“…Surgical reports have recorded neural edema and swelling in cases of BP, 2,4 which are supported by findings of increased enhancement (particularly at the geniculate ganglion and along the labyrinthine segment) on MRI 29 . The second, “compressive theory,” suggests that swelling of the nerve within the bony canal leads to neural entrapment, increased endoneural pressure and vascular congestion, ischemia, impairment of axoplasmic flow, axonal degeneration and then necrosis 7,27,30,31 …”

“…Although considered idiopathic and a diagnosis of exclusion, a number of factors have been proposed for the potential underlying pathophysiology for BP, including anatomical variants, viral infection, ischemia, inflammation, autoimmunity and environmental conditions. 27 , 28 These hypotheses can by broadly categorized into two groups; either patients develop recurrent BP due to recurrent episodes of pathological inflammation within an anatomically normal bony canal or they are susceptible to episodes of BP due to a narrow LFN canal. Surgical reports have recorded neural edema and swelling in cases of BP, 2 , 4 which are supported by findings of increased enhancement (particularly at the geniculate ganglion and along the labyrinthine segment) on MRI.…”

“… 29 The second, “compressive theory,” suggests that swelling of the nerve within the bony canal leads to neural entrapment, increased endoneural pressure and vascular congestion, ischemia, impairment of axoplasmic flow, axonal degeneration and then necrosis. 7 , 27 , 30 , 31 …”

Nasal Herpes Simplex With Infraorbital Neuralgia: A Rare Presentation

“…Herpes simplex can rarely accompany facial nerve palsy. HSV-1 becomes latent in the sensory neurons and can reactivate due to factors like cold, fever, stress, ultraviolet exposure, menstruation, orofacial trauma/surgery, and immunosuppression [ 12 , 13 ].…”

Clinical Implication of Facial Nerve Decompression in Complete Bell’s Palsy: A Systematic Review and Meta-Analysis

“…Although various mechanisms, including viral infections, vascular ischemia, and immune-mediated processes, have been suggested to contribute to Bell’s palsy [24,25], the exact pathophysiology of Bell’s palsy has not yet been clearly elucidated. In anatomical perspectives, the diameter of the meatal segment of the facial nerve is small (approximately 0.68 mm) at the point where it enters the fallopian canal and is susceptible to inflammation and edema [26]. Thus, the edematous swelling of the fallopian canal which underlies Bell’s palsy decreases the room for expansion in a rigid bony canal [27], potentially leading to severe nerve damage and even necrosis and fibrosis.…”