FIG. 4.
Possible neurophysiological mechanisms of secondary HFS according to tumor pathology. A: Cardiac-related pulsatile CSF flow changes lead to pulsatile movement of the arachnoid cyst leading to facial nerve compression (blue arrowheads). Pulsatile stretching of the facial nerve causes demyelination and induces activation of voltage-gated and mechanosensitive ion channels (blue arrowheads).28 B: An epidermoid cyst encasing or attaching to the facial nerve. Cholesterol in the tumor stimulates the facial nerve and induces HFS (red arrows).33,34 C: The vestibular schwannoma is attached to the facial nerve without an arachnoid membrane; however, the schwannoma insulates the facial nerve.32 The tumor anchors to the internal auditory meatus. Less pulsatile stretching of the facial nerve occurs with cardiac-related pulsatile CSF flow changes. D: Meningiomas attach to the petrous surface. Less pulsatile stretching of the facial nerve occurs with cardiac-related pulsatile CSF flow changes.