A 67-year-old woman was referred to the department of ophthalmology of our institution with a 4 month history of headache, intermittent vertical diplopia, and fluctuating left upper lid ptosis, which was often worse in the afternoon (Fig. 1). She had a history of systemic hypertension.FIG. 1: A. At presentation, left upper lid ptosis and frontalis overaction are evident. B. Later in the day, the left upper lid ptosis has increased.Best-corrected visual acuity was 20/60 in each eye. Ocular motility examination in the right eye was normal. In the left eye, there was a very variable and apparently fatigable ptosis, with palpebral fissures measuring 6 mm on the left and 10 mm on the right. Abduction, adduction, and infraduction were normal in the left eye, but supraduction was reduced to approximately one-third of the normal range. There were no pupillary abnormalities. The rest of the ophthalmologic examination was unremarkable, as was the neurologic examination. Three days later, anisocoria was first noted, with the right pupil measuring 4 mm in dim illumination and reacting briskly to light and the left pupil measuring 6.5 mm and reacting sluggishly to light. There was no relative afferent pupillary defect. MRI and magnetic resonance angiography (MRA) showed a 22.5 mm diameter saccular aneurysm arising from the cavernous and supraclinoid segment of the left internal carotid artery (Fig. 2). The patient was offered coiling but declined.FIG. 2: A. Postcontrast T1 coronal MRI shows a 22.5 mm diameter mass in the left cavernous sinus with supracavernous extension. B. Shaded surface display magnetic resonance angiography shows that the aneurysm arises from the cavernous and supraclinoid segment of the left internal carotid artery.Aneurysmal third cranial nerve palsy is usually caused by aneurysms that arise from the junction of the internal carotid artery and posterior communicating artery (89%) but can be caused from aneurysms located in the intracavernous internal carotid artery (6.2%), as found in our patient, or in the basilar artery (3.4%), posterior cerebral artery, or superior cerebellar artery (1,2). In patients with aneurysmal third cranial nerve palsy, pupillary reactions are usually affected first, followed by ptosis, and finally extraocular muscle paralysis affecting the medial, superior, and inferior rectus and oblique muscles (2,3). Ptosis caused by aneurysmal third cranial nerve palsy is usually not variable (1). The marked fluctuation in ptosis seen in our patient has been reported only rarely (4). It has been attributed to intermittent hyperfunction of the muscles supplied by the third cranial nerve. Coexisting inappropriate neural discharge with blockage is the presumed mechanism (4). The presence of fluctuating unilateral ptosis in an elderly patient with minimal extraocular muscle dysfunction and pupil-sparing does not rule out intracavernous aneurysmal compression. Sonia Attia, MD Sonia Zaouali, MD Chahira Chourabi, MD Amel Boughammoura, MD Riadh Messaoud, MD Mahbouba Frih, MD Moncef Khairallah, MD Department of Ophthalmology (SA, SZ, RM. MK) Department of Neurology (AB, MF) Fattouma Bourguiba University Hospital Monastir, Tunisia [email protected]
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Apr 7, 2009
Fernando Ruiz-Juretschke + 6
Open Access