Bela Ajtai1, Ed J Fine, Norah Lincoff. 1. Department of Neurology, State University of New York at Buffalo, NY, USA. ajtaix@yahoo.com
Abstract
BACKGROUND: Oculomotor nerve paresis may have relatively benign but also life-threatening causes. Distinguishing between these is of great clinical importance. OBJECTIVE: To reveal a potential pitfall of the clinical evaluation of oculomotor nerve paresis. PATIENT: Single case observation. RESULTS: A 56-year-old man had fluctuating diplopia and fatigable ptosis, promptly relieved by intravenous edrophonium, leading to the diagnosis of ocular myasthenia gravis. His pupillary function was intact. A few days after the initial diagnosis, he suffered a subarachnoid hemorrhage secondary to the rupture of a basilar artery aneurysm. His ocular symptoms were related to aneurysmal oculomotor nerve compression. CONCLUSION: Patients with oculomotor nerve dysfunction need more detailed evaluation because the underlying cause cannot be safely determined on a clinical basis.
BACKGROUND:Oculomotor nerve paresis may have relatively benign but also life-threatening causes. Distinguishing between these is of great clinical importance. OBJECTIVE: To reveal a potential pitfall of the clinical evaluation of oculomotor nerve paresis. PATIENT: Single case observation. RESULTS: A 56-year-old man had fluctuating diplopia and fatigable ptosis, promptly relieved by intravenous edrophonium, leading to the diagnosis of ocular myasthenia gravis. His pupillary function was intact. A few days after the initial diagnosis, he suffered a subarachnoid hemorrhage secondary to the rupture of a basilar artery aneurysm. His ocular symptoms were related to aneurysmal oculomotor nerve compression. CONCLUSION:Patients with oculomotor nerve dysfunction need more detailed evaluation because the underlying cause cannot be safely determined on a clinical basis.