Table 4.

Summary of key evidence for the etiological theory about immune inflammatory

Key references	Summary of evidence
[57]	Histologic changes in the facial nerve, found by Liston and Kleid, that can be summarized as follows:(1) the nerve, from the internal acoustic meatus to the stylomastoid foramen, is infiltrated by round, small inflammatory cells. (2) There was A breakdown of neuron myelin sheaths, which involved macrophages, occurs. (3) Inter-neuronal space increased. (4) The bony fallopian canal is normal, with no sign of facial nerve compression by the fallopian canal bone
[60–63]	In recent years, it is found that the mean neutrophil-to-lymphocyte ratio and neutrophil values were higher in adult and pediatric patients with Bell’s palsy
[64, 65]	Similar changes in peripheral blood leukocyte subpopulations are also described in the process of a few inflammatory demyelinating diseases, such as during the acute stage of Guillain–Barré syndrome and in acute exacerbations of multiple sclerosis. Bell’s palsy, such as Guillain–Barré syndrome, may be an acute demyelinating disease of the peripheral nerve system
[68]	An examination of the serum samples from patients with Bell’s palsy showed elevated concentrations of cytokines interleukin-6 (IL-6), interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-α) were increased compared with control groups
[69, 70]	In contrast to control populations, decreased percentages of total T cells (CD3) and T helper/inducing cells (CD4) have also been found in the acute phase of the disease. An obviously decreased peripheral blood T lymphocyte percentages and an increase in B lymphocyte percentage in BP have been found within the first 24 days from the clinical onset of the paralysis. These evidences indicate an activation of cell-mediated effectors and the involvement of immune mechanisms in Bell’s palsy