Bell's palsy pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Possible mechanisms
- The majority of patients with blepharospasm have a high incidence of local ocular symptoms prior to or at the onset of blepharospasm, such as blepharitis, conjunctivitis, dry eyes or photophobia.
- Chronically disturbed sensory inputs to the central nervous system due to lagophthalmos and corneal irritation may contribute to the generation of blepharospasm.
- In patients with Bell’s palsy, there is an enhanced blink reflex secondary to inputs from the paralyzed side compared which those of the non-paralyzed side.
- Abnormal afferent input from the paralyzed side contributes to the abnormal sensitization of the blink reflex, thus facilitating the induction of abnormal facial motor outputs such as blepharospasm.
- It is unclear why Bell’s palsy-induced blepharospasm is extremely rare.
Microscopic Pathology
- The facial nerve has an edematous, thickened perineurium with infiltrates of inflammatory cells between nerve bundles and around blood vessels.
- It appears that the histology of the facial nerve in Bell's palsy is similar to Herpes Zoster infection, suggestive of an infectious cause.