Endocrine Abstracts

Background: It is estimated that 1-6% of patients with a pituitary adenoma develop ocular nerve palsies. These are primarily due to tumour extension into the cavernous sinus and most commonly affect the 3^rd cranial nerve. Because of its sheltered position within the sinus, the 6^th cranial nerve is rarely affected. When this does occur, it most commonly results from ischemic neuropathy secondary to diabetes, hypertension or mononeuritis multiplex.

Case report: A 35-year-old male presented with a one-month history of double vision on looking left. He described symptoms as worse in the mornings, particularly after a night of sleeping on his left-hand side. Formal visual field examination showed no field defects, but a left 6th cranial nerve palsy was clearly demonstrated. No other neurological defects were elicited and physical examination was unremarkable save for enlarged hands and frontal bossing. A diagnosis of acromegaly was confirmed with an oral glucose tolerance test which showed failure to suppress growth hormone below 0.3mcg/L. IGF-1 levels were measured at 109 nmol/L. Further testing revealed an impaired fasting glucose with an Hba1c of 6.2% and a short synacthen test showed an inadequate rise in the cortisol response. Other pituitary functions were unimpaired and an autoimmune screening was negative. ESR was within the normal range. An MRI of the pituitary revealed a large non-enhancing sellar lesion with marked extension into the left parasellar territory. This abutted the left cavernous segment and encompassed the left 5^th and 6^th nerves. The MRI showed no evidence of infarction. The patient was immediately commenced on oral hydrocortisone and depot injections of lantreotide. Review of symptoms two weeks later showed moderate improvement of the diplopia, however resection of the tumour will require neurosurgical intervention.

Discussion and conclusion: Pituitary adenoma should be considered as a differential in a patient presenting with a 6^th cranial nerve palsy. In this case, although the cranial nerve palsy most likely resulted from direct compression by the adenoma (as suggested by the MRI), it is possible that an ischaemic neuropathy occurred secondary to impaired glucose metabolism.