“…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.…”