Hyperprolactinaemia and the empty sella.

side-effects in this patient. In addition, symptomatic changes in taste were different between the anterior two-thirds and the posterior one-third of the tongue. This contrast was attributed to the different degree of recovery between the anterior part, which is innervated by the chorda tympani, and the posterior part, which is innervated by the glossopharyngeal nerve, suggesting a dysfunction of the bilateral chorda tympani and glossopharyngeal nerves. Paroxysmal facial spasms and abnormal enhancement of the genua portion also supported the involvement of facial nerves. Therefore, we concluded that the hypogeusia in this patient was caused by cranial nerve neuropathies. In this patient, hypogeusia developed after a long history of peripheral polyneuropathy. Previous pathological studies have described patients with a long-standing course who have developed cranial nerve symptoms.8,9 These patients have suggested that cranial nerves are vulnerable to the autoimmune mechanism in CIDP, and that the symptoms resulted from the combination of demyelination and axonal degeneration in the cranial nerves. In conclusion, hypogeusia may occur in patients with CIDP with long disease duration as one of the manifestations of cranial nerve involvement. Immunosuppressive therapy may be effective for the hypogeusia as well as the usual neuropathic symptoms of CIDP.