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Show Journal of C/ ini, al NeurO- OI, htllQ/ nr" It'gy 10( 1 j 56- 58. 1990. Transient Partial Oculomotor Nerve Paresis with Posterior Communicating Artery Aneurysm A Case Report ttl 1990 Raven Press, Ltd., New York Beverly N. Greenspan, Ph. D., M. D., and Alexander G. Reeves, M. D. A 38- year- old woman is described who developed a partial right oculomotor paresis which cleared spontaneously prior to clipping of an associated nonhemorrhagic bilobate right anterior communicating artery aneurysm. Key Words: Reversible oculomotor paresis- Cerebral aneurysm. Department of Medicine. Section of Neurology, DartmouthHitchcock Medical Center, Hanover, New Hampshire, U. S. A. Address correspondence and reprint requests to Dr. A. G. Reeves, Section of Neurology. Dartmouth- Hitchcock Medical Center, Hanover, NH m75f>, U. S. A 56 Aneurysms of the posterior communicating artery produce oculomotor nerve palsy in - 30- 40% of cases, and about half of these are without concomitant subarachnoid hemorrhage ( 1,2). Aneurysm of the internal carotid or distal basilar arteries also may present as painful oculomotor palsy, sometimes with only minimal signs ( 3). We report a case in which the oculomotor paresis associated with an aneurysm resolved spontaneously. CASE REPORT A 38- year- old woman presented with a complaint of a severe right retroorbital throbbing headache that had been constant for 2 weeks. She also complained of blurred vision in the right eye, beginning a few days after the onset of the headache. She had intermittent nausea, vomiting, anorexia, and photophobia during the headache. Examination revealed no meningismus. Visual acuity was 20/ 25- 1 in the left eye and 20/ 40- 1 ( without improvement with pinhole) in the right eye at distance. There was slight ptosis of the right eye. The pupils were 4 mm and equal and reactive to light and accommodation, and extraocular movements were intact. The examination was otherwise unremarkable. Lumbar puncture produced clear, colorless cerebrospinal fluid with no white cells, 24 red cells, a protein of 34 mgldL and glucose of 55 mgldL. A tapering course of prednisone was prescribed. One week later she had no change in her headache, blurred vision, or intermittent nausea and vomiting, and she complained of vertical diplopia on upgaze. Examination showed more pronounced ptosis of the right eye and evidence of a TRANSIENT PARTIAL OCULOMOTOR NERVE PARESIS 57 right superior rectus palsy. The right pupil was larger than the left by < 1 mm, and both pupils reacted briskly to light. Visual acuity was unchanged. The remainder of the examination, including fundoscopic exam, corneal reflex testing, and test of afferent pupillary defect, was unremarkable. A contrast- enhanced computed tomography ( CT) scan of the head with 3- mm cuts through the base of the brain did not show any abnormalities. A telephone conversation with the patient 10 days after she was first seen elicited that her headache and visual symptoms were without change. When next seen 5 days after this, she said her blurred vision and vertical diplopia were gone, although the headache was unchanged. Examination revealed complete resolution of previously observed signs. The next day cerebral angiography revealed a bilobate posteriorly directed 6- 8- mm aneurysm of the right posterior communicating artery ( PCoA) projecting posteriorly from the junction of the PCoA and the supraclinoid portion of the internal carotid ( Fig. 1). Uneventful surgical obliteration of the aneurysm was performed. COMMENT Partial oculomotor palsy due to unruptured intracranial aneurysm of the internal carotid artery near the takeoff of the PCoA or of the basilar artery has been reported ( 3), but except for one report of transient mild ptosis with an unruptured internal carotid- PCoA junction aneurysm ( 4), we know of FIG. 1. Right carotid angiogram showing posterior communicating artery aneurysm. no report of oculomotor palsy of this etiology that resolved over days or weeks. In the case mentioned ( 4) there was also progressive mydriasis of the affected eye. Gale and Crockard ( 5) reported a case of transient unilateral mydriasis with a basilar artery bifurcation aneurysm directed toward the relevant third nerve. This case differs from ours in that their patient had definite hemorrhage from the aneurysm with seizures, meningeal signs, papilledema, and blood in the ventricles shown by CT scan of the brain. The mydriasis was present for only 1 hat 16- 17 h after the hemorrhage, and possibly represented an early transient sign of transtentorial herniation, as the patient clearly had dilated ventricles and increased intracranial pressure at that time. Walsh and Hoyt ( 6) state " some oculomotor palsies caused by aneurysms will disappear without treatment," but they cite no examples. A few untreated patients included in old series showed recovery of oculomotor palsy over years, often with signs of aberrant regeneration of the third cranial nerve ( 7- 9). Small PCoA aneurysms can also readily cause oculomotor palsy since they lie close to the course of the nerve, and are said in a recent review ( 10) to be the most common single cause of isolated oculomotor palsy. Ptosis is typically the first symptom of an initially incomplete paresis and may be preceded by ipsilateral headache ( 1), as in this case. The levator palpebrae is also the first muscle to recover function after surgical treatment of aneurysms, but the superior rectus shows the least postoperative recovery ( 2,7). In our patient both these muscles were clinically involved and both recovered before treatment. More commonly, the initially partial oculomotor palsy due to aneurysm becomes complete 2- 3 days after onset ( 1,10,11). The pupil is usually involved but may be spared ( 11- 15). PCoA aneurysms that produce oculomotor palsy may be large, and as in our case, multiloculated ( 2). Possibly the resolution of the deficits in our patient was due to the pressure of the aneurysm causing a conduction block rather than axon degeneration, as postulated by Hamer ( 1) to account for postoperative resolution. The aneurysm may have been expanding and may have shifted slightly in position as it grew, pressing only transiently on the third cranial nerve. As stressed by Bartleson et al. ( 3) and Hamer ( 1), oculomotor palsy when caused by aneurysm may be an important warning sign of hemorrhage, which in Okawara's ( 16) six patients with aneurysmal " extraocular muscle impairment," occurred at a mean of 29.6 days after onset of this symptom. His data came from retrospective studies of pa- I elin Neuro- ophthalmol, Vol. 10, No. 1, 1990 58 B. N. GREENSPAN AND A. G. REEVES tients who had hemorrhage, however, and so do not represent the incidence of subarachnoid hemorrhage in patients who present with oculomotor palsy. Nonetheless, our case shows that the possibility of aneurysm as a cause of oculomotor palsy and ipsilateral headache must be considered even when the ocular symptoms resolve over the next weeks. In 1946 Jefferson ( 7) wrote ' The difference between [ ophthalmoplegic migraine] and aneurysmal compression is that in the periodic palsies the nerve usually recovers so completely that an entirely fresh palsy is possible and may be repeated time after time. In the aneurysms the recovery after a single episode is never complete enough for so strikingly fresh a palsy to present itself." Our patient initially was treated with prednisone as for migraine " status," but it is difficult to attribute the resolution of her ocular findings to this, since at the time she completed a lO- day course of prednisone her symptoms were unchanged. Her case demonstrates that oculomotor deficits secondary to aneurysm may not only be incomplete ( 3), but may be transient. REFERENCES 1. Hamer J. Prognosis of oculomotor palsy in patients with aneurysms of the posterior communicating artery. Acta Neurochir 1982; 66: 173- 85. 2. Soni SR. Aneurysms of the posterior communicating ar: tery and oculomotor paresis. J Neurol Neurosurg Psychiatry 1974; 37: 475-- 84. 3. Bartleson JO, Trautmann JC, Sundt TM Jr. Minimal oculomotor nerve paresis secondary to unruptured intracranial aneurysm. Arch NeuroI1986; 43: 1015- 20. 4. Payne JW, Adamkiewicz J Jr. Unilateral internal ophthalmoplegia with intracranial aneurysm. Am J Ophthalmol 1969; 68: 349- 52. 5. Gale AN, Crockard HA. Transient unilateral mydriasis with basilar aneurysm. J Neural Neurosurg PsychiJ: Itry 1982; 45: 565- 6. 6. Walsh FB, Hoyt WF. Clinical Neuro- Ophthalmology, 3rd ed., Vol. 2. Baltimore: Williams and Wilkins, 1969: 1764. 7. Jefferson G. Isolated oculomotor palsy caused by intracranial aneurysm. Proc R Soc Med 1946; 40: 419- 32. 8. Henderson JW. Intracranial arterial aneurysms. A study of 119 cases, with special reference to the ocular findings. Trans Am Ophthalmol Soc 1955; 53: 349- 62. 9. Cantu RC, Souders T, Helper RS. Effects of carotid ligation on aneurysm- induced oculomotor palsy. J Neurosurg 1969; 31: 528-- 32. 10. Maurice- Williams RS. Subarachnoid hemorrhage. Bristol, UK: Wright, 1987: 121- 2. 11. Kissel JT, Burde RM, Klingele TG, et al. Pupil- sparing oculomotor palsies with internal carotid- posterior communicating artery aneurysms. Ann Neural 1983; 13: 149- 54. 12. Green WR. Neuro- ophthalmologic evaluation of oculomotor nerve paralysis. Arch OphthalmoI1964; 72: 154- 67. 13. Raja I. Aneurysm- induced third nerve palsy. J Neurosurg 1972; 36: 548-- 51. 14. O'Connor PS, Tredici TJ, Green RP. Pupillary- sparing third nerve palsy due to aneurysm: a survey of 2419 neurological surgeons. JNeurosurg 1983; 58: 792- 3. 15. Kasoff I. Kelly OL. Pupillary sparing in oculomotor palsy from internal carotid aneurysm. JNeurosurg 1975; 42: 713- 7. 16. Okawara S- H. Warning signs prior to rupture of an intracranial aneurysm. , Neurosurg 1973; 38: 575- 80. |
