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Year : 1985  |  Volume : 33  |  Issue : 5  |  Page : 327-329

Ophthalmoplegia cavernous sinus syndrome

Department of Neuro Surgery, S.C.B. Medical College Cuttack Orissa, India

Correspondence Address:
Madhumati Misra
Department of Neuro Surgery, S.C.B. Medical College, Cuttak Orissa
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Source of Support: None, Conflict of Interest: None

PMID: 3843346

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How to cite this article:
Misra M, Rath S. Ophthalmoplegia cavernous sinus syndrome. Indian J Ophthalmol 1985;33:327-9

How to cite this URL:
Misra M, Rath S. Ophthalmoplegia cavernous sinus syndrome. Indian J Ophthalmol [serial online] 1985 [cited 2021 Apr 19];33:327-9. Available from: https://www.ijo.in/text.asp?1985/33/5/327/30742

Most of the intracranial aneurysms are usually detected after the first subarachnoid haemorrhage associated with cranial nerve signs[1],[2],[3]. However, there exists a small group of so called "giant aneurysms" of more than 2.5 cm in diameter where the warning subarachnoid leak is absent and most of the symptoms are produced by its mass. Such aneurysms in the anterior cavernous sinus may involve the IIIrd nerve alone or all the ocular motor nerves may be involved. Encroachment of the middle cavernous sinus is indicated by involvement of the V 1 & V 2 sensory roots. However, combined involve­ment of the 2nd, 3rd, 4th, V 1 & V 2 and VIth­cranial nerves with nonpulsatile exophthal­mos, orbital oedema and papilloedema due due to impaired orbital venous drainage caused by a growing intracavernous carotid aneurysm is extremely rare[3],[4]. The nature of such aneurysmal growth is still unknown and seems to be due to two facts : real enlargement of its sac and thinning of its wall from episodes of clinically unnoted bleeding. Balance of both processes result in aneurysmal growth. Dominance of one of them results either in bleeding or in arrest of growth[1],[2],[5].

We describe a girl who presented features of orbital cellulitis and the underlying giant intracavernous internal carotid artery aneurysm was not promptly recognised as the contributing factor due to its rarity. The diagnosistic difficulties encountered and the timely surgical intervention that saved both life and vision prompted us to offer the following case report.

  Case report Top

A 14 year old girl was first seen for head­ache, retrobulbar pain and lid oedema on the left side for the previous 2 days. Ocular examination revealed features of left orbital cellulitis, the globe was tender and fixed. Left pupil was reacting sluggishly. Best corrected visual acuity was 6/5 OD and 6/60 OS. Slit lamp examination of the anterior segment was normal in both eyes. No cells in the posterior vitreous could be detected on contact lens examination. Ophthalmoscopy revealed a normal disc on the right side and the left disc appeared chocked with peripa­pillary retinal oedema, A course of systemic antibiotic was instituted.

The patient's condition worsened over the subsequent 2 days and headache was intensi­fied. Re-examination revealed left sided facial oedema with chemosis, Left V 1 & V 2 sensory loss. semidilated ad fixed pupil and visual loss to no perception of light. The left globe was proptosed and tender. Slit lamp examination of anterior chamber and poste­rior vitreous was still unremarkable. Right optic disc was normal on ophthalmoscopy the left disc was acutely chocked with massive peripapillary retinal haemorrhage. Such findings were again thought to be consistent with acute orbital inflammation with optic neuritis.

The patient had a complete general physi­cal examination which did not reveal a septic focus. A complete blood count, erythrocyte sedimentation test and urine analysis were normal. CT showed a rounded mass with abnormal uptake of contrast medium alongside the sella on the left side, the mass was enlarging the superior orbital fissure and eroding the basisphenoid [Figure l]a, b. No orbital pathology could be shown in CT scan.

Left carotid angiography demonstrated an unruptured giant intracavernous carotid aneurysm [Figure - 2]. Right carotid angiogram demonstrated adequate collateral circulation to the opposite hemisphere. Internal carotid ligation in the neck was performed after Matas compression test[6] and orbital signs regressed within 10 days of surgery. Repeat CT showed marked increase in attenuation values of the aneurysm, reflecting complete thrombosis[7]. Absorption co-efficient were similar to those of clotted blood[7] (80 Houns­field unit). The patient is asymptomatic till the day of last report and visual acuity in the left eye 15 months after surgery has improved to appreciation of hand movement at close range.

  Discussion Top

Orbital cellulitis is usually the result of spread of infection from the paranasal sinuses and anterior orbit, and may be due to a variety of organisms, of which staphylococcus and streptococcus are the commonest[5]. Response to systemic antibiotics is dramatic in early stages, Localised abscess and super­iosteal collections require surgical drainage.

Lesions in the retro-orbital, parasellar and cavernous sinus regions may involve ocular nerves and vessels in their intracranial course, and present confusing clinical signs as occurred in the present case[2],[3],[4]. Progres­sively enlarging intracaverncus aneurysm initially cause VIth nerve palsy and this may be followed later by signs of IIIrd and IVth nerve palsy. Finally the Vlth nerve is invol­ved, and upward extension may produce visual loss. The evolution of these changes have been fully documented by Barr et al[3] and the case illustrated here shows these features terminating in a blind eye. Acuteness of the disease with features of gross papilloedema and orbitofacial oedema suggest acute expansion of a pre-existing asympto­matic aneurysm within the cavernous sinus. CT and carotid angiography con­firmed the extent of the lesion and excluded an concomittant orbital pathology.

Giant aneurysm of the internal carotid artery present difficult problem[6],[9]. Although good result can be obtained with direct microsurgical attack, cervical carotia ligation with or without bypass procedure remain a valid treatment for these lesions[6],[7],[8]. The effects of carotid ligation have been moni­tored by CP recentiy[9]. Giant aneurysms may be divided into 3 types, partially throm­bosed, completely thrombosed and not thrombosed[7].

On plain CT scan, aneurysms that are not thrombosed appear sharply delineated with a slightly increased homogenous density. Partially thrombosed aneurysms appear as areas of mixed density and a completely thrombosed aneurysm presents as a rounded area with mottled appearance and calcified wall[7]. Following contrast medium infusion, the lumen shows intense enhancement while the thrombosed part remains unchanged. Successful result of carotid ligation can be immediately displayed on post operative CT scan by an intense increase in attenuation values of the aneurysm, which assumes the absorption co-efficient of clotted bloods. However, cerebral angiography continues to play an important role in the pre-operative work up of giant aneurysms[5],[7],[9].

It seems that our case of unruptured giant intracaveinous carotid artery aneurysm presenting as signs like orbital cellulitis is an extremely unusual finding and a review of current literature failed to show a similar case. The purpose of this report is to alert ophthalmologists to certain pitfalls in the diagnosis of primary orbital afflictions.

  Summary Top

We report the case of a girl who develop­ed features of left orbital cellulitis with rapid amaurosis. Computed tomographic scan (CT) demonstrated an ipsilateral retro orbital/parasellar high dense mass and carotid angiography showed it to be an unruptured giant aneurysm (3 cm diameter) of intra­cavernous internal carotid artery. Prompt internal carotid ligation in neck was life saving and resulted in resolution of orbital symptoms.

  References Top

Pick, J. Line, D.P, Bock, W.J., 1983, Surg. Neu­rol, 20, 288.  Back to cited text no. 1
Ramamurty, B.. 1980, Intracranial aneurysms. In Ramamurty, B, and Tandon, P,N. Ed Text book of neurosurgery, Vol. I, India National book trust, 1980 p. 501.  Back to cited text no. 2
Barr, H.W.K. Blackwood, W. and Meadows S.P., 1971, Brain, 94,607.  Back to cited text no. 3
Mancuso, AA Hansfee, W. N. Winter, J. and Ward P., 1978, Neuroradiology, 16:449.  Back to cited text no. 4
Rath, S. and Mishra, M,, 1982, Ind. J. Ophthal­mol,, 30:157.  Back to cited text no. 5
Pozzati, E. Fagioli, L. Servadel, F, and Gaist G., 1981, J. Neurol. Surg, 55:527.  Back to cited text no. 6
Raymond, D.A. and Tew, J., 1978, J. Neurosurg Psych., 41:83.  Back to cited text no. 7
Gelber, B R. Sundt T.M. Jr. 1980, J. Neuro­surg., 52,1.  Back to cited text no. 8
Schubiger, A. Valavanis, A. Hayek J., 1980, J. Comput. Assist. Tomogr , 4:24.  Back to cited text no. 9


  [Figure - 1], [Figure - 2]


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