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Year : 1982  |  Volume : 30  |  Issue : 3  |  Page : 157-160

Aneurysm induced ophthalmoplegia

Department of Neurosurgery, S.G.B. Medical College, Cuttack, India

Correspondence Address:
Sanatan Rath
Department of Neurosurgery, S.G.B. Medical College, Cuttack-7
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Source of Support: None, Conflict of Interest: None

PMID: 7174062

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How to cite this article:
Rath S, Misra M. Aneurysm induced ophthalmoplegia. Indian J Ophthalmol 1982;30:157-60

How to cite this URL:
Rath S, Misra M. Aneurysm induced ophthalmoplegia. Indian J Ophthalmol [serial online] 1982 [cited 2021 May 8];30:157-60. Available from: https://www.ijo.in/text.asp?1982/30/3/157/28198

A case of left oculomotor palsy due to posterior communicating artery aneurysm is presented for its rarity among intracranial aneurysms. Such patients might seek ophthal­mic advice initially for acute ipsilateral ocular palsy. If a leaking aneurysm is not suspected, the associated symptoms of headache, vomit­ing, neck pain and unconsciousness due to subarachnoid haemorrhage could be ignored and the ophthalmoplegias are taken as benign. Such patients are often followed up with con­servative treatment. Without neurosurgical interference, severe rebleeding is possible within the 7th to 21st day following an usual "warning leak" and this episode may kill the patient[1],[2],[3] It is estimated that 15% of cases with aneurysm induced ophthalmoplegia, treated conservatively, die of recurrent bleed­ing within first 24 hours, an additional 50% die within the first 8 weeks[2]. In contrast, emergency surgery following contrast angio­graphy, undertaken within few days, is life saving[3].

Hence, recognition of aneurysm-induced­ ophthalmoplegia is important in ophthalmic practice to arrange urgent neurosurgical referral and appropriate treatment in time.

  Case report Top

AP, a 45 year old Hindu female was admitted to the neurosurgical unit on with the complaints of sudden drooping of left upper eye lid since 3 days. The illness started 5 days back with left sided frontal headache, retro-orbital pain and bouts of vomitting. She became gradually disoriented within few hours and was admitted to a neighbouring hospital in an unconscious state.

Positive physical findings recorded in the first hospital included a state of unconscious­ness responding to painful stimuli, mild neck stiffness and complete oculomotor palsy in the left side. Blood pressure was 140/90 mm of Hg. and pulse rate was 82 per minute. General physical examination and neurological exami­nation revealed no other abnormality. Availa­ble ophthalmic findings were complete left oculomotor palsy with normal funds picture in both the eyes. All routine labora­tory tests were within normal limits. Diagno­stic lumbar puncture revealed haemorrhagic CSF.

Because of the sudden onset, preceding left sided headache and ipsilateral oculomotor palsy, a leaking left supraclinoid aneurysm was suspected. Her sensorium improved with conservative treatment, without any improve­ment of oculomotor function and was referred to us for further care.

The physical, neurological and ophthalmo­logical examinations were otherwise normal except mild neck stiffness and complete oculo­motor palsy on the left side [Figure - 1].

The ptosis on the left side was complete and crossed diplopia could be demonstrated.

On lifting the left upper lid manually. The false image was higher with its upper end tilted towards the left side. I he right pupil was 2 mm in diameter and normally reactive. The left pupil was 5 mm in diameter and are flexic to light (direct and consensual) and convergence. Vision in both eyes were 20/20. She could read J3 print at 30 cm. distance with the right eye and required + 3.OD addi­tion to read J3 print with the left eye. The accommodation such estimated in the left eye was + 3.0 Diopters less than that in her right eye. Other ophthalmic investigations as Schi φtz tonometry, exophthalmometry, slit lamp examination, ophthalmoscopy, periphe­ral and central fields were all within normal limits.

Routine laboratory studies revealed no abnormality. Blood VDRL test was negative. Serum Cholesterol level was 200 mg. '/,, and fasting blood sugar, 86 mg. %. The lumbar CSF was Xanthochromic, cytology showed few red cells and the biochemistry was within normal limits. Plain X-ray of skull, chest and PNS were unremarkable.

Left carotid angiogram demonstrated an aneurysm at the junction of left posterior communicating artery and internal carotid artery [Figure - 1]C. A simultaneous right carotid angiogram excluded multiple aneurysms, other congenital anomalies in the supratento­rial circulation and proved the adequacy of collateral circulation prior to carotid ligation in the affected side.

As an operative procedure, left common carotid ligation in the neck was performed after "Matas compression test" proved ade­quate functional circulation in the brain. The patient was discharged on the 8t$ post opera­tive day with the ocular state remaining un­changed.

At a recent check up after 6 months, ptosis had recovered by 50%, the left palpe­bral fissure measuring 5 mm, while the right measured 9 mm. The left pupil was 4 mm in diameter and sluggishly reacting to light and convergence. The right pupil however measured 2 mm in diameter with normal reacti­vity. The estimated accommodation in the left eye was still 1.5 diopters less than that of the right eye. The movements in the extraocu­lar muscles supplied by left oculomotor nerve have partially recovered and anomalous associa­tions have not developed yet. The patient has been asymptomatic till the day of last report.

  Discussion Top

Aneurysms of posterior communicating artery are rare and reported to be 1 - 4% of intracranial aneurysms[2],[4], the incidence being still lower in India[5].

The earliest report of intracranial aneurysm was by Hutchinson[6] and since the discovery of cerebral angiography, aneurysms of intra­cranial vessels are being increasingly recogni­sed.

The association of intracranial aneurysms with hypertension, diabetes, arthrosclerosis and intracranial infection are described[1],[2],[6]. But in majority of cases, the condition is thought to be congenital, due to developmental defects in the elastic coat and muscle coat of the vessel wall[1]. Such aneurysms are com­moner among females and manifest after middle age[6],[8], left sided affection is encoun­tered more often[7], as has been seen in the present case.

Acute unilateral pain on the side of the aneurysm and referred around the eye is the presenting feature in 90% of cases[7], pain starts before the aneurysm ruptures when a minor leak from the fundus of the sac occurs into the subarachnoid space and induces local meningeal reaction[8],[9]. The sac becomes pro­gressively thin and ruptures finally.

Acute, ipsilateral and complete oculomotor palsy is produced due to kinking of the oculo­motor trunk at its emergence from the mid brain between the posterior cerebral artery and the posterior superior cerebellar artery[2],[9]. Associated factors like thrombosis of the nutri­ent vessels and the degree of stretching of the nerve over the aneurysmal sac contributes not only to the paralysis, but also the progress of recovery. A large haemorrhage may act as a space-occupying-lession and produce palsies due to displacement or pressure upon the nerve.

Pupilloplegia is associated in 70-90% of cases[3],[8],[10], due to the peripheral and superior placement of pupillomotor fibers in the oculo­motor nerve trunk, which make them more susceptible to extrinsic pressure from an aneurysms[9]. The same has been seen in the present case.

Following surgery, full ocular movements rarely return and anomalous associations may develop due to irregular regeneration of the axons along terminal branches of the ocular motor nerve[8],11. As the posterior vessels supply principally the optic radiation and visual cortex, field defects are usually associa­ted with posterior communicating artery aneurysm, but may be absent where the optic radiation is protected by collateral blood supply[1]. No functional defect, either in the acuity or field of vision was noted in the present case.

The classical signs of meningeal irritation such as headache, vomiting and unconscious­ness with ipsilateral oculomotor palsy suggest leaking intracranial aneurysm. Blood in the CSF on lumber puncture confirms the diagno­sis. Contrast cerebral angiography localises the aneurysm, defines its connection and the extent of collateral circulation prior to surgery[4],[8].

All cases of leaking aneurysms demand urgent neurosurgical interference. Proximal ligation of the common carotid artery in the neck is an accepted and safe procedure. The head pressure within the aneurysmal sac is thus reduced and the fear of rebleeding is prevented.

Direct intracranial approach for oblitera­tion of the aneurysm is often hazardous and leads to rupture of friable aneurysmal sac during dissection, but with the development of modern micro-neuro-vascular surgery, more such cases are being attacked directly.

Recovery of oculomotor function post­operatively, as has been seen in this patient, occurs only in 5% cases. Better recovery is expected if the surgery is undertaken within the first 10 days.

  Summary Top

A case of leaking posterior communicating aneurysm in an elderly female, presenting as ipsilateral rotal accumulator palsy is reported for its rarity. Aspects of neuro ophthalmic diagnosis followed by successful neurosurgical intervention, resulting in fair recovery of oculomotor function are discussed.

  References Top

Drake, C.G., 1971, Proc. roy. Soc. Med. 63:477.   Back to cited text no. 1
Gillingham F.J. 1958-Ann. of Roy. Col. Surg. Eng. 23:89.  Back to cited text no. 2
Jefferson, G., 1946, Proc. roy. Soc. med. 40:419.  Back to cited text no. 3
Griffith H.B., Cummins. B.H., Thomson, J.L.G. 1972 Jr. Neuro. radiology 4: 212.  Back to cited text no. 4
Reddy, Raja D., Pravakar, V, and Rao Dayananda, B., 1972, Neurology India. 20.8.  Back to cited text no. 5
Reddy G., Reddy, Raja, Muraliwhhar and Rajyalaxmi 1979, Ind. J. Ophthalmol. 27:212.  Back to cited text no. 6
Hutchinson, 1875, quoted by Mohanty B. and Rath S. 1970. The Ind. Practitioner 23:645.  Back to cited text no. 7
Green W.R., Hackett. E.R., Schlezinger N.S. 1964 Arch. Ophthalmol. 72, 154.  Back to cited text no. 8
Duke Elders, S., 1971, System of Ophthalmology Vol. XII. Henry Kimpton London pp. 772.  Back to cited text no. 9
Payne, J.W. and Adamkiewiez J„ 1969, Amer. J. Ophthalmol. 68:349.  Back to cited text no. 10


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