Bell's palsy is the most common type of peripheral facial nerve palsy and it is often preceded by dysgeusia. The facial palsy is induced by damage throughout peripheral facial nerve fibers. However, reduced gustation in the early stages of Bell's palsy could result from damage of the geniculate ganglion cells as well as the peripheral nerve fibers. In order to clarify the pathogenesis of dysgeusia observed in cases of Bell's palsy, ultrastructural changes in the geniculate ganglion cells were observed in three ischemic facial palsy models. Ischemia was induced in guinea pigs by; 1) permanent interruption of the petrosal branch of the middle meningeal artery, 2) freezing of the upper tympanic part of the facial nerve canal using dimethylether liquid propane gas, without exposure of the facial nerve bundle, 3) temporary ligature of the carotid arteries after permanent interruption of both the vertebral arteries and petrosal branch of the middle meningeal artery of guinea pigs. Severe peripheral facial palsy was seen in all of the three ischemic models by 7 days after surgery. However, ultrastructural changes were observed in several light cells of the geniculate ganglion only in the model using freezing. Cytoplasmic changes included the degeneration of ganglion cell nuclei and the accumulation of myeloid bodies in nerve fibers. The findings suggest that the dysgeusia observed in cases of Bell's palsy could be mainly induced by complete ischemia of local facial nerve canal.