The pathogenesis of Bell's palsy is presented as retrograde epineurial compression edema with ischemia of the facial nerve. Although the etiology is unknown, an attractive theory is vasospasm, from any cause, along any facial nerve branch, with the chorda tympani, perhaps, the usual primary involvement. Retrograde vascular distension and edema, within the epineurium of the bony facial canal, compresses the nerve from outside its perineurial sheath. The compression force may be mild or severe, resulting in varying degrees of reversible or irreversible ischemic degeneration of myelin sheaths and axons, with varying degrees of cellular reaction to myelin breakdown. The edema may be resorbed, leaving reversible or irreversible nerve damage, or may stimulate collagen formation within the epineurium, with persisting fibrous compression (entrapment) neuropathy of the facial nerve. This concept is consistent with the varying results of Bell's palsy, and depends on the severity and duration of edema, and whether fibrosis occurs within the epineurium of the facial canal. Epineurial fibrosis also results in disturbance of metabolic exchange through the epineurial-permeurial-endoneurial tissues, and may ultimately result in obliteration of vascular drainage. Two temporal bone cases of Bell's palsy, one occurring ten years before death, with residual paralysis. and one two years before death, with clinical recovery, are added to the previously described four cases in the literature, three of early Bell's palsy, and one of remote palsy with almost complete recovery.
Differences in the Diameter of Facial Nerve and Facial Canal in Bell’s Palsy—A 3-Dimensional Temporal Bone Study
