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Show Journal of Clinical Neuro-ophthalmology 13(4); 229-231, 1993. Isolated Palsy of the Superior Branch of the Oculomotor Nerve Due to Chronic Erosive Sphenoid Sinusitis Leonidas Stefanis, M.D. and Serge Przedborski, M.D., ph.D. © 1993 Raven Press, Ltd., New York We report one case with isolated unilateral superior branch oculomotor nerve palsy due to an erosive sphenoid sinusitis. Within 8 weeks after surgical drainage of the sphenoid sinusitis, the patient recovered fully from the superior branch oculomotor palsy. In view of the dramatic clinical improvement that followed surgery, we hypothesized a compression of the superior branch of the oculomotor nerve by the sphenoidal abscess. To our knowledge, this is the first reported case of a superior branch oculomotor nerve palsy related to an erosive sinusitis and cured by sinusotomy, a safe and simple surgical procedure. Thus, we believe that our observation bears some practical implications of clinical importance in the management of patients who present partial oculomotor nerve palsy. Key Words: Superior branch oculomotor nerve palsyErosive sphenoid sinusitis. From the Department of Neurology, College of Physician & Surgeons, Columbia University, New York, New York, U.S.A. Address correspondence and reprint requests to Dr. Serge Przedborski, Black Bldg., Room 307, Department of Neurology, 650 West 168th Street, New York, NY 10032, U.S.A. 229 Nontraumatic pupil-sparing oculomotor nerve palsy is most commonly due to ischemic infarction. On rare occasions, it can also be due to compression of the superior branch of this nerve by either a neoplasm or an aneurysm in the anterior portion of the cavernous sinus (1). We report on a patient who presented with a oculomotor nerve superior branch palsy, which completely recovered after drainage of a sphenoid sinus abscess. CASE REPORT This 80-year-old woman with a history of hypertension and intermittent atrial fibrillation, presented with a 2-week history of severe diffuse headache associated with nausea, decreased appetite, chills, and insomnia. The patient denied any recent fever, ear-nose-throat infection, or visual problems. A year ago, however, she had an acute onset impairment of vision in the right eye likely due to central retinal vein occlusion. On admission, the patient was in marked distress due to severe headache. She had a normal physical and neurologic examination, except for a visual acuity of 20/100 in the right eye (patient's baseline in the past year). Fundoscopy showed a macular hole in the right eye and bilateral arteriovenous nicking; no pallor was noted. Blood cell counts and glucose were normal. ESR was 28-38 mmlh. Cerebrospinal fluid protein level was 40 mg/dl and there was 1 leukocyte/mm3 . A brain computed tomography (CT) scan with contrast-enhancement was considered normal. Radiographs of the paranasal sinuses did not show evidence of sinusitis, but the sphenoid sinuses were not well visualized. On day 7, the patient developed a right ptosis associated with supraorbital pain. On day II, in addition to progressive worsening of the ptosis, she also had restriction of elevation in abduction of the right eye 230 L. STEFANIS AND S. PRZEDBORSKl with diplopia. The other extraocular movements were intact. The pupils were 3 mm, symmetric, and reacting well to light and accommodation. There was no conjunctival injection or proptosis. The visual acuity remained the same. Corneal reflex and facial sensations were normal. Tensilon test was negative. Magnetic resonance imaging (MRI) of the head, with gadolinium, showed an opacified right sphenoid sinus of heterogeneous consistency with some enhancement. Sphenoid sinus abnormalities were, in retrospect, present on the previous CT scan. On day 14, a CT scan of the paranasal sinuses showed thickening of the sphenoid sinus wall, opacified right sphenoid sinus, and erosion of the optic canal (Fig. 1A). The patient was started on cefuroxime, and on the following day, a right sphenoid sinusotomy was performed and about 5 ml of frank pus was collected. Cultures were positive for Staphylococcus aureus but remained sterile for fungus. Cytology for malignant cells was negative. On the following day, the pain subsided, and the ptosis was reduced. Three weeks later, there was complete recovery of the right eye and eyelid movements and a resolution of the right sphenoid sinus opacification on CT scan (Fig. 18). DISCUSSION Our patient's clinical picture is characterized by an isolated weakness of the right levator palpebrae and superior rectus resulting from an involvement of the superior branch of the ipsilateral oculomotor nerve. We believe that the abscess was the offending factor, since the patient's deficit improved after the right sphenoid sinus was drained. In addition, the erosion of the optic canal seen on CT suggests that the earlier impairment of vision was due to an involvement of the optic nerve by this infectious process. However, the exact location of the oculomotor nerve involvement remained uncertain, since it has been shown that similar divisional palsies can occur at any point along the route of the nerve, even proximal to its branching in the anterior cavernous sinus (2,3). In our case, it is likely that the lesion was, indeed, proximal to the cavernous sinus, since we did not observe any clinical signs in favor of cavernous sinus syndrome. Although sinusitis has been implicated in a few cases of pupil-sparing third nerve palsy (4,5), often associated with involvement of the optic nerve, it did not appear as a possible cause of oculomotor nerve palsy in any of the extensively referenced large Mayo Clinic series (Cr8). We believe that this etiology might be underestimated and unrecog- J Clin Neuro-ophthalmol, Vol. 13, No.4, 1993 FIG. 1. Computed tomography scan of the head. (A) Coronal view of sphenoid sinuses prior to sinusotomy showing opacification of the right sphenoid sinus with erosion of the optic canal (arrow). (B) Coronal view of sphen~id sinuses 2 months after sinusotomy showing resolution of the opacification of the right sphenoid sinus (at this time the patient had a complete recovery of her right eye and eyelid movements). nized, and we recommend ruling out inflammatory/ infectious processes of the sinuses by using the appropriate imaging studies before proceeding to an angiography (9) in cases of oculomotor nerve palsy, especially those involving preferentially the superior branch. REFERENCES 1. Trobe JD. Isolated third nerve palsies. Semin NeuroI1986'6: 135-41. ' 2. Guy J, Savino P, Schatz NJ, Cobbs WH, Day AL. Superior division paresis of the oculomotor nerve. Ophthalmology 1985;92:777-S4. OCULOMOTOR NERVE PALSY 231 3. Brazis PW. Localization of lesions of the oculomotor nerve: recent concepts. Mayo Clin Proc 1991;66:1029-35. 4. Green WR, Hackett ER, Schlezinger NS. Neuro-ophthalmologic evaluation of oculomotor nerve paralysis. Arch OphthalmoI1961;72:154-67. 5. Johnson LN, Hepler RS, Yee RD, Batzdorf U. Sphenoid sinus mucocele (anterior clinoid variant) mimicking diabetic ophthalmoplegia and retrobulbar neuritis. Am / Ophthalmol 1986;102:111-5. 6. Rucker CWo Paralysis of the third, fourth and sixth cranial nerves. Am / OphthalmoI1958;46:787-94. 7. Rucker CWo The causes of paralysis of the third, fourth and sixth cranial nerves. Am / Ophthalmol 1966;61:1293--8. 8. Rush JA, Younge BR. Paralysis of cranial nerves III, IV, and VI; cause and prognosis in 1000 cases. Arch Ophthalmol 1981;99:76-9. 9. Trobe JD. Isolated pupil-sparing third nerve palsy. Ophthalmology 1985;92:58--61. 1Clin Neuro-ophthalmol, Vol. 13, No.4, 1993 |
