The role of facial canal diameter in the pathogenesis and grade of Bell's palsy: a study by high resolution computed tomography

Abstract

We found the diameter of labyrinthine segment of facial canal as an anatomic risk factor for Bell's palsy. We also found significant relationship between the HB grade and FC diameter at the level of second genu. Future studies (MRI-CT combined or 3D modeling) are needed to promote this possible relevance especially at second genu. Thus, in the future it may be possible to selectively decompress particular segments in high grade BP patients.

The etiology of Bell’s palsy: a review

“…In their more detailed study, Celik et al [13] found that the facial canal's mean width at the labyrinthine section in the affected temporal bone was much smaller than the respective one in the unaffected side (p = 0.00). In that retrospective clinical study, the authors used temporal computed tomography and found no notable differences between the affected and unaffected temporal bones at the geniculate ganglion, second genu, tympanic segment, mastoid segment, and the stylomastoid foramen except for the labyrinthine segment.…”

“…There is a significant difference between influenced and uninfluenced sides of the patients in terms of the mean CSA of the FN and IAC (p < 0.001). Bell's palsy seems to usually coincide with the narrower fallopian tube of the patient [13,14] The mean width was significantly smaller at the labyrinthine section of the facial canal in the influenced temporal bone than the equivalent in the uninfluenced (p = 0.00) [14] Significant relationship was found between the HB grade and the facial canal diameter at the level of second genu (p = 0.02) [9] In patients with higher primary HB-scores, their 6-month later HB-scores were also higher. In patients with higher 6-month HB score; their IAC inlet and mid-canal values were lower Table 2 Summary of key evidence for the etiological theory about virus infection Key references Summary of evidence [21][22][23][24] The α-HV which target peripheral neurons (e.g., HSV-1, HSV-2, and VZV) can establish lifelong infections and infectivity potential in the host including in the autonomic and sensory ganglia of the head, neck and cranial [25] Reactivation of HSV-1 centered around the geniculate ganglion was first outlined by McCormick in 1972 [26] The presence of HSV-1 deoxyribonucleic acid (DNA) was detected in clinical specimens, i.e., intra-temporal facial nerve endoneural fluid in Bell's palsy patients [27][28][29] Animal models have the capability to cause facial paralysis through initial infection and virus reactivation incited by immune modulation [36,37] Earlier work examining cellular electrophysiology in the setting of herpes infection demonstrated a pathway for the quick and dynamic control of excitability in sensory neurons by internalization of sodium channels.…”

Evaluation of the facial nerve and internal auditory canal cross-sectional areas on three-dimensional fast imaging employing steady-state acquisition magnetic resonance imaging in Bell’s palsy

“…In a recent study, the width of the facial canal (FC) on temporal bone computed tomography (CT) was found to be smaller at the meatal foramen and at the middle part of the labyrinthine segment of the FN on the affected sides of BP patients (14). In another CT study that investigated the role of FC diameter in BP patients, the width at the labyrinthine segment of the FC was found to be significantly smaller in the affected temporal bones (15). However, as the authors of that study stated, only measuring the FC Table 3.…”

Paralisia facial unilateral: aspectos clínicos e principais tratamentos

“…A paralisia de Bell é uma síndrome clínica idiopática, caracterizada por desenvolvimento espontâneo de uma paralisia unilateral dos músculos inervados pelo nervo facial (Louis; Mayer; Rowland, 2018) e que são responsáveis pelas expressões faciais (Tortora;Derrickson, 2016). Esta condição é a causa mais comum de lesão desse nervo (Louis;Mayer;Rowland, 2018), com uma incidência de 20 a 30 pessoas por 100.000 por ano (Celik et al, 2017). Ela atinge todas as faixas etárias, com uma frequência ligeiramente maior entre a terceira e quinta década de vida.…”

“…Além disso, tende a afetar igualmente os dois lados da face e suas recidivas são raras (Louis;Mayer;Rowland, 2018). As causas possíveis incluem infecção pelo herpes-vírus simples (HSV) (Tortora;Derrickson, 2016), edema do nervo facial por conta da inflamação, neuropatia isquêmica, insuficiência da microcirculação (Celik et al, 2017), diabetes e hipertensão (Louis;Mayer;Rowland, 2018).…”