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Bell's Palsy Pathology

It is thought that as a result of inflammation of the facial nerve, pressure is produced on the nerve where it exits the skull within its bony canal, blocking the transmission of neural signals or damaging the nerve. Patients with facial palsy for which an underlying cause can be found are not considered to have Bell's palsy ''per se''. Possible causes include tumor, meningitis, stroke, diabetes mellitus, head trauma and inflammatory diseases of the cranial nerves (sarcoidosis, brucellosis, etc.). In these conditions, the neurologic findings are rarely restricted to the facial nerve. Babies can be born with facial palsy. In a few cases, bilateral facial palsy has been associated with acute HIV infection.

In some research the herpes simplex virus type 1 (HSV-1) was identified in a majority of cases diagnosed as Bell's palsy. This has given hope for anti-inflammatory and anti-viral drug therapy (prednisone and acyclovir). Other research however, identifies HSV-1 in only 31 cases (18 percent), herpes zoster (zoster sine herpete) in 45 cases (26 percent) in a total of 176 cases clinically diagnosed as Bell's Palsy. That infection with herpes simplex virus should play ''a major role'' in cases diagnosed as Bell's palsy therefore remains a hypothesis that requires further research.

In addition, the herpes simplex virus type 1 (HSV-1) infection is associated with demyelination of nerves. This nerve damage mechanism is ''different'' from the above mentioned - that oedema, swelling and compression of the nerve in the narrow bone canal is responsible for nerve damage. Demyelination may not even be directly caused by the virus, but by an unknown immune system response. The quote below captures this hypothesis and the implication for other types of treatment:

It is also possible that HSV-1 replication itself is not responsible for the damage to the facial nerves and that inhibition of HSV-1 replication by acyclovir does not prevent the progression of nerve dysfunction. Because the demyelination of facial nerves caused by HSV-1 reactivation, via an unknown immune response, is implicated in the pathogenesis of HSV-1-induced facial palsy, a new strategy of treatment to inhibit such an immune reaction may be effective. and Epstein-Barr viruses, both of the herpes family. Reactivation of an existing (dormant) viral infection has been suggested suggest that this new activation could be preceded by trauma, environmental factors, and metabolic or emotional disorders, thus suggesting that stress - emotional stress, environmental stress (e.g. cold), physical stress (e.g. trauma) - in short, a host of different conditions, may trigger reactivation.

Further Reading


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