| OCR Text |
Show ] ourtUll of Clinical Neuro- ophtluJlmology 10( 1): 5~ 1, 1990. Ptosis as the Sole Manifestation of Compression of the Oculomotor Nerve by an Aneurysm of the Posterior Communicating Artery Edward F. Good, M. D. © 1990 Raven Press, Ltd., New York Oculomotor palsy secondary to a berry aneurysm is usually present with pupillary dilatation, followed by other signs of third cranial nerve dysfunction, including oculomotor paresis and ptosis. Partial paralysis of the nerve with pupil sparing has been observed, but ptosis as the sole sign of oculomotor paralysis has not previously been reported until now, Key Words: Berry aneurysm- Oculomotor PalsyPtosis. Dr. Good is a neurologist in private practice. Address correspondence and reprint requests to Dr. Edward F. Good, 450 Blossom Street, Webster, TX 77598, U. S. A. 59 Compression of the oculomotor nerve ( third cranial nerve) in the subarachnoid space almost always presents with pupil dilatation and other signs of third nerve dysfunction, including ptosis and external ophthalmoparesis, If due to an aneurysm, facial and orbital pain are also present, Recent reviews point out the frequent occurrence of partial and minimal palsies, particularly with pupil sparing ( 1,2). I report a patient who developed a headache and ptosis as the sole manifestation of compression of the oculomotor nerve by a saccular aneurysm of the posterior communicating artery. CASE REPORT A 42- year- old woman had the insidious onset of a left frontal and retroorbital headache that was progressive. After 1 week, the pain became so severe that she ceased working. At that time, she noted drooping of the left upper lid. A computed tomography ( CT) scan of the head was performed, which was normal. Two weeks later, she consulted an ophthalmologist. There was no diplopia reported with a red lens test. Cover- uncover testing was orthophoric for distance, with a small degree of exophoria at near. Versions were full. The pupils were 3 mm and reacted briskly, directly, and consensually. Palpebral fissures measured 8 mm 00 and 6.5 mm as. A diagnosis of acquired ptosis was made. A neurological consultation was requested because of the severe headaches. The patient denied any double vision or other neurological symptoms. Internal and external function of the oculomotor nerve again was normal with the exception of a left- sided ptosis. A review of old photographs ( Figs, 1 and 2) did not reveal any evidence of ptosis. 60 E. F. GOOD FIG. 3. Postsurgery. because of the peripheral dorsomedial location of the pupillomotor fibers within the nerve. Walsh and Hoyt ( 3) state that pressure anywhere along the basilar segment of the third nerve produces pupillary dilatation, and this effect is not dependent on the topography of the pupillary axons within the nerve. Pupil sparing of the oculomotor nerve has been reported along any portion of the nerve, but is most common in the cavernous sinus ( 1,4). Partial third nerve paralysis of an external type implies ptosis and decreased range of motion in the appropriate direction of the muscles innervated by the third nerve with or without deviation from the primary position. In several recent reviews of ptosis and third cranial nerve lesions, it has been stated that an isolated unilateral ptosis should not be regarded as a sign of an oculomotor paralysis (~ 7). To my knowledge, there are no reported cases of isolated ptosis attributed to the compression of the oculomotor nerve. Isolated ptosis without pain is probably rarely compressive; however, the association of ipsilateral headache with acquired ptosis, as in other partial third cranial nerve palsies, should alert one of the possibility of an intracranial aneurysm and should prompt careful follow- up and possible use of other diagnostic modalities. CT scanning reportedly may miss up to a third or more of these lesions ( 2). ( It is uncertain what percentage would be picked up by MRI, and angiography remains as the only definitive test to elucidate this lesion.) It is difficult to explain the late, i. e., postoperative, onset of double vision. In 6 of 12 of Bartelson's patients, third nerve dysfunction was worse postoperatively. Faulty clip placement, clip slippage, operative disection, and hemorrhages have been reported as possible causes ( 8). Acknowledgment: I would like to thank Victor J. Basso, M. D., for evaluation and referral of this patient. COMMENT Because of the intractable headache, an angiogram was performed. The study revealed a large bilobed aneurysm of the posterior communicating artery. At operation, the oculomotor nerve was found to be compressed by the aneurysm, with fresh clot in the dome. There was evidence of old bleeding by the presence of hemosiderin pigment and xanthochromia. The third nerve was encased by an old hematoma and fresh thrombus. The patient made an uneventful recovery, but her ptosis persisted ( Fig. 3). Several weeks postoperatively, the patient noted double vision on extreme right gaze and downgaze. A red lens test at that time revealed an exophoria on right gaze and a left hyperphoria on downgaze. The pupils remained equal. FIG. 1. Old photograph 0:' pat; snt s!" l, O". v; ng no ptosis. The cardinal signs of an oculomotor palsy are ptosis, mydriasis, and extraocular motion paralysis. Bartleson et al. ( 2) reported 12 cases of minimal oculomotor paralysis secondary to unruptured intracranial aneurysms. In each of these cases, at least one element of oculomotor dysfunction was absent. Mydriasis and ptosis were equally common as signs of third nerve paralysis followed by dysfunction of the extraocular muscles. Mydriasis alone occurred in one patient. Mydriasis is generally the most common first sign of oculomotor compression and is generally considered to occur FIG. 2. Photograph of patient taken before angioqram PTOSIS RESULTING FROM ANEURYSM 61 REFERENCES 1. Kissel JT, Burde RM, Klingele TG, Zeiger HE. Pupil- sparing oculomotor palsies with internal carotid- posterior communicating artery aneurysms. Ann Neurol 1983; 13: 149- 54. 2. Bartleson JT, Trautmann Je, Sundt TF. Minimal ocular motor nerve paresis secondary to unruptured intracranial aneurysm. Arch NeuroI1986; 43: 1015- 20. 3. Walsh FB, Hoyt WF. Clinical neuro- ophthalmology. Baltimore: Williams & Wilkins, 1969: 252. 4. Nadeau SE, Trobe JD. Pupil sparing and ocular motor palsy: a brief review. Ann NeuroI1983; 13: 14>- 8. 5. Thurston SE. Differential diagnosis of third cranial nerve palsies. Neuro View 1987; 3: 1- 5. 6. Lepore FE. Ptosis and disorders of eyelid opening. Neurol Neurosurg Update Ser 1986; 7: 1- 7. 7. Trobe JD. Third nerve palsy. Neurol Neurosurg Update Ser 1985; 6: 1- 7. 8. Wakai S, et al. Ocular motor palsy caused by aneurysm clip: report of two cases. Neurosurgery 1981; 9: 429- 32. I Clin Neuro- ophthalmoI, Vol. 10, No.!, 1990 |
