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Show Journal ( if Nnim- Ophllidliimlony 19( 1): 46- 48, 1999. © 1999 Lippincoll Williams & Wilkins, Inc., Philadelphia Inferior Division Third Nerve Paresis From an Orbital Dural Arteriovenous Malformation Lawrence G. Gray, o. D., Steven L. Galetta, M. D., Beverly Hershey, M. D., A. Charles Winkelman, M. D., and Alan Wulc, M. D., F. A. C. S Isolated inferior division third nerve palsies are rare. The authors report a patient with an isolated, pupil- involving inferior division third cranial nerve palsy from an intraorbital dural arteriovenous malformation. Despite spontaneous thrombosis of the malformation, the third nerve palsy persisted. To the authors' knowledge, this is the first case report of an inferior division third nerve palsy caused by an orbital dural arteriovenous malformation. Key Words: Inferior division third cranial nerve paresis- Orbital dural arteriovenous malformation ( AVM)- Superior orbital fissure- Superior ophthalmic vein- Exophthalmos. Manuscript received July 27, 1998; accepted October 30, 1998. From the Departments of Neurology ( L. G. G., A. C. W.), Ophthalmology ( L. G. G., A. C. W., A. W.), and Radiology ( B. H.), Hahneman University, and the Department of Neurology ( L. G. G., S. L. G.), University of Pennsylvania Medical Center, Philadelphia, Pennsylvania. Address correspondence and reprint requests to Steven L. Galetta, M. D., Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104. Fourteen cases of inferior division third cranial nerve palsies have been reported in the English literature. Etiologies include trauma, vasculitis/ demyelination, virus, metastasis, brainstem arteriovenous malformation ( AVM), mesencephalic ependymal cyst, inflammation, and idiopathic etiologies ( 1- 7). Orbital dural AVMs represent less than 0.5% of all orbital masses ( 8). Dural AVMs are usually found in the posterior fossa and cavernous sinus and may expand to the orbit. We report an orbital AVM as the cause of an inferior division oculomotor paresis. CASE REPORT A 39- year- old woman was told by her coworkers that she had an enlarged right pupil. Six weeks before examination, an ophthalmologist noted anisocoria and a non-reactive right pupil that constricted to 0.125% pilocarpine ophthalmic solution. Three weeks before examination, the patient's right eye became tender to touch, and she developed double vision. The tenderness subsided, but the diplopia persisted. Neuro- ophthalmic examination showed a limitation of the right inferior rectus, FIG. 1. Paresis of the inferior division of the right third cranial nerve. Notice the absence of ptosis, a right hypertropia, and a nonreactive pupil in the primary position. There is a slight right hypertropia in right gaze and right adduction deficit in left gaze. Both eyes elevate normally in gaze up and to the right. A left hypertropia of 15 prism diopters was measured in gaze up and to the left. An underaction of the right inferior rectus is evident in gaze down and to the right. 46 INFERIOR DIVISION THIRD NERVE PARESIS 47 D / • : Vir'- 4 wJr V^^ H?** _ H^ I ' MPs? ' ' • I : 1 r M l • 4-. * 1 •, i FIG. 2. A: Axial T1 - weighted image shows a lesion isointense to muscle in the posterior orbit extending through the superior orbital fissure ( white arrow) in the right posterior orbit. B: Axial T1- weighted contrast- enhanced fat suppression magnetic resonance image demonstrates marked enhancement of the lesion ( black arrow) consistent with a dilated posterior portion of the right superior ophthalmic vein. C: Coronal T1- weighted noncontrast fat suppression magnetic resonance image shows the splaying of the origin of the lateral rectus muscle from the supraorbital and infraorbital tendon ( white arrows). A small arrow indicates vessels related to the dural AVM. D: Coronal T1- weighted magnetic resonance image anterior to ( C) shows the single lateral rectus muscle ( white arrow), and there is minimal dilation of the ophthalmic venous system inferior to the optic nerve. E: Lateral view of right internal carotid arteriogram shows enlargement of the meningeal branch of the ophthalmic artery ( straight arrow) feeding the dural arteriovenous malformation ( curved arrow). 48 L. G. GRAY ETAL. right medial rectus, and right inferior oblique muscles. ( Fig. 1). There was no ptosis, and the levator function of both eyelids was 16 mm. There were 45 prism diopters of right exotropia in primary gaze. The patient was ortho-phone in gaze up and to the right. Fifteen prism diopters of left hypertropia were measured in left and upgaze, and 15 prism diopters of right hypertropia were measured in right and down gaze. There were more than 45 prism diopters of exotropia in left gaze and 8 prism diopters of exotropia in right gaze. There was no adduction or retraction of the eye on attempted vertical movement. Forced ductions were negative. Three millimeters of anisocoria were noted without a relative afferent pupillary defect in ambient room illumination. The right pupil was fixed to light, but constricted segmentally on attempted convergence. The pupil constricted to 0.125% pilocarpine ophthalmic solution. There was 4 mm of right exophthalmos on Hertel exophthalmometry. Ophthalmoscopy was normal. Visual acuity was 20/ 20 OU. Visual field and color vision testing was normal. Applanation tensions were OD 16 and OS 14 mm of Hg without exaggerated ocular pulsations. No bruits were auscultated over the orbit or posterior auricular regions. Corneal sensation was normal, and there were no other focal neurologic signs. Magnetic resonance imaging showed a dilated, enhancing superior ophthalmic vein consistent with slow flow or acute thrombosis. ( Fig. 2, A and B). Coronal Tl showed the splaying of the origin of the lateral rectus muscle tendon by the engorged ophthalmic vein. On a more anterior coronal Tl image, the lateral rectus muscle appeared as a single structure. ( Fig. 2, C and D). A carotid angiogram performed 5 weeks later demonstrated an intraorbital dural arteriovenous malformation supplied by the recurrent meningeal, a branch of the ophthalmic artery, draining to the cavernous sinus. ( Fig. 2E). The dilated superior ophthalmic vein was not demonstrated at the time of the arteriogram compatible with thrombosis. There was no clinical change at the 12- month follow- up examination. DISCUSSION Both inferior division third nerve paresis and orbital dural AVMs are uncommon. This case represents the first report of a dural orbital AVM and its secondary varix causing an inferior division third cranial nerve paresis. Orbital AVMs present with a pulsatile exophthalmos, vascular congestion, and chemosis ( 9). Our patient had exophthalmos without any other signs of orbital congestion. A dilated pupil was the initial presentation of our patient's intraorbital dural AVM. Segmental iris sphincter paresis, tonic pupillary contraction upon convergence, and supersensitivity to 0.125% pilocarpine ophthalmic solution were consistent with a tonic pupil ( 10). Preserved corneal sensation implies sparing of the ciliary ganglion. This suggests that the cause of the tonic pupil was localizable to the short ( motor) root to the ciliary ganglion ( 11, 12). The painful 3- week progression from a tonic pupil to the onset of diplopia suggests expansion of the AVM to involve the inferior branch of the third cranial nerve. The coronal Tl- weighted image ( Fig. 2C) shows a splaying of the annular origin of the belly of the lateral rectus muscle from the supraorbital and infraorbital tendon by an engorged ophthalmic vein. This implies that the inferior division of the third nerve may have been compressed as it passed through the annulus of Zinn to the superior orbital fissure ( 13,14). The superior division was probably spared because it separates from the inferior division and is located in a more protected rostral position. The mechanism of our patient's inferior division third cranial nerve paresis remains uncertain. The initial finding of a tonic pupil exophthalmos, followed by the evolution of a painful, inferior division third nerve paresis, suggests a compressive etiology. Although we cannot completely exclude engorgement of the extraocular muscles, the negative forced ductions, the pupil involvement, and the magnetic resonance imaging findings make this less likely. The failure of the paresis to recover over 12 months makes an ischemic mechanism less tenable. REFERENCES 1. Susac JO, Hoyt WF. Inferior branch palsy of the oculomotor nerve. Ann Neurol 1977; 2: 336- 9. 2. Cross AG. 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