Pathology of Bell's Palsy

Observations on Melkersson’s syndrome

“…As it descends the aqueduct it increases in thickness and strength which reaches a maximum in density and tough-ness as it approaches the stylomastoid foramen. When the Fallopian canal is explored for compression and the facial sheath slit, the nerve laterally herniates through the incision (Ballance & Duel, 1932;Morris, 1938;Cawthorne, 1951;Kettel, 1947;Sullivan & Smith, 1950), and is seen to be markedly congested and swollen to twice its normal size (Hall, 1951). This process is particularly marked in the lower third of the canal.…”

“…It would appear that the role of the Fallopian canal in facial paralysis is a secondary mechanical one, superimposing adverse pressure effects with consequent ischaemia upon an already existing neurological injury, only when the nerve swells to a size that can no longer be accommodated comfortably in such a restricted and unresilient channel. The bone around the stylomastoid foramen, and that of the mastoid itself, share in the pathological changes, and at operation softening is seen in this area, which particularly affects the tip of the mastoid process and its air cells (Kettel, 1947;Flodgren, 1946;Hall, 1951). This softening is likely to be a bony necrosis due to ischaemia, since a stem vessel from the stylomastoid artery enters the foramen, and branches from it pass through the posterior wall to supply the air cells of the mastoid process.…”

“…These branches will suffer compression if the nerve is swollen. The nerve as well as the sheath is involved in an inflammatory reaction as it passes the bony portion of the Fallopian aqueduct (Rothlander, 1953;Hall, 1951), and in severe cases peripheral atrophy occurs. The actual agent which causes the nerve to swell and initiate the above chain of events is yet a matter for conjecture.…”