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Show ]. Clin. Neuro-ophthalmol. 1: 225-229, 1981. Ophthalmoplegia due to Spontaneous Thrombosis in a Patient with Bilateral Cavernous Carotid Aneurysms ROBERT RAPPORT, MD, F, REED MURTAGH, MD, Abstract A case of acute onset of right ocular ophthalmoplegia which is felt to be, on angiography, the result of thrombosis of a documented right cavernous sinus aneurysm, is presented. Possible pathophysiologic basis for this unusual finding is presented. Introduction A 53-year-old white male with documented bilateral cavernous carotid aneurysms experienced acute onset of right ocular ophthalmoplegia which was studied by angiography and computed tomography (CT) and felt to result from thrombosis of the right cavernous aneurysm, The pathophysiologic association of the clinical and radiographic findings is discussed. To the best of our knowledge no such case has previously been reported. Case History This 53-year-old white male with a previous history of hypothyroidism, hypertension, and chronic renal failure secondary to polycystic renal disease began to experience diplopia and mild dull pain over his right eye approximately 15 months prior to his admission to James A. Haley Veterans Administration Hospital in Tampa, Florida. On neurologic examination, cranial nerves II to XII were found intact but the patient reported mild diplopia. Carotid angiography revealed the presence of bilateral intracavernous carotid artery aneurysms, saccular and measuring 2 cm in diam- From the Department of Radiology, University of South Florida College of Medicine (RR, FRM), and the Division of Neuroradiology of the 1.A. Haley Veterans Administration Hospital, Tampa, Florida (FRM). September 1981 eter on the right and fusiform with a l-cm diameter on the left (Fig. 1). Surgery was felt not to be indicated. During an admission 2 years later for hemodialysis, he experienced sudden onset of right sixth nerve paralysis, mi(jsis, absent sensation in the distribution of first division of the right trigeminal nerve and absent right corneal reflex. Unenhanced CT scan of the brain revealed a mass of increased density in the right parasellar area representing the right cavernous sinus aneurysm, Figures la-Ie. AP (a) and lateral (b) views of selective right carotid angiogram in 1978 show aneursym of the right cavernous carotid which completely fills the cavernous sinus. (c). Selective left carotid angiogram demonstrates smaller left cavernous sinus aneurysm in lateral projection. 225 Sponl,lI1C'ous Thrombosis (b) (e} Figure J (continued). largl'r than on CT 2 yl'ars prl'viously (Fig. 2). The smailldt-sidl'd anl'urysm was unch.mged. Bil.~teral ,.HoliJ .Hleriogr.lm reve,lled thrombosis of the right carotid cavernous sinus ,1Iwurysm with pat~'" " 'or ,,' .... illlra',lVernous 'i'orti,)J1 of the right 220 carotid artery. (Fig. 3) The thrombosis apparently coincided with and was responsible for the sudden onset of symptoms. The left-sided aneurysm had not changed significantly from the prior study. Neurosurgical intervention was felt not to be in- Journal of Clinical Neuro-ophtholmolgy Rapport, Murtagh Figure 2. CT scan of the brain with contrast in 1980 admission shows large right, smaller left densities representing carotid cavernous aneurysms. dicated. The patient was discharged with persistent right ophthalmoplegic changes and diplopia. Discussion Intracavernous carotid aneurysms compromise approximately 5_6%1 of all aneurysms and occur chiefly in individuals over age 40 who have a history of vascular hypertension.2 Approximately 8% of intracavernous aneurysms produce bony erosion and about one third demonstrate calcification: Five percent are bilateral, as in our case. Pressure from the aneurysm may occlude or displace the internal carotid artery, and occasional rupture of these aneurysms into the cavernous sinus can produce a carotid cavernous fistula with consequent cephalic bruit, pulsatile exophthalmos and ocular palsy. If rupture of a carotid cavernous aneurysm does not occur in the early stages, expansion of the aneurysm gradually brings the aneurysm wall into contact with the cavernous sinus dural covering as was seen on the original angiogram in our case. This mechanism is felt to provide protection against rupture.2 Compression of the nerves of the cavernous sinus can also occur during the process of expansion with involvement of the third, fifth, and sixth cranial nerves in their course through the cavernous sinus. Involvement of the sixth cranial nerve is almost always the first clinical feature, and may be the sole abnormality for a long period of time. It has September 1981 been postulated that this occurs because the sixth nerve is in closest physical apposition to the carotid artery and is unsupported by fibrous covering. The third cranial nerve is usually next to be involved temporarily with associated neurological findings of ptosis, impaired elevation and adduction of eye, plus sluggish pupillary reaction. A mid-dilated pupillary size has been attributed to involvement of ocular sympathetic fibers surrounding the internal carotid artery. Trigeminal sensory loss in divisions I and II is regarded as a classical sign of intracavernous aneurysms, but this usually presents late in the clinical course. When the trigeminal nerve is physically compressed, pain may occur as a prominent symptom. Our case involved a patient with bilateral cavernous sinus aneurysms who presented initially with mild diplopia. It was not until 2 years later that the other clinical signs of intracavernous .meurysm, (i.e., right sixth nerve paralysis, loss of sensation in the first division of the fifth nerve, .lbsent right corneal reflex and miosis of right pupil) manifested themselves. Because the appearance of these symptoms and signs was sudden, the demonstrated thrombosis of the right-sided cavernous sinus aneurysm was felt to be responsible. Although the presence of laminated clot occurring in carotid cavernous aneurysm has been previously described,2 the clot is thought to have a function of protection against rupture of the aneu- 227 Spontaneous Thrombosis (b) Figures 3.1 and 3b. AP .md Idterdl views of right selective right cdrotid dngiogrdm in 1980 shows obliterdtion of the right Cdvemous dneurysm except for d chdnnel of (dVernOUs cdrotid which remdins dnd supplies well the intrdcrdnidl brdnches. left-sidt'd dnt'urysm WdS unchdnl\ed. rysm. We propose that in this particular instance, the intracavernous aneurysmal thrombus acted to compromise further the vascular supply to the i'1V()I\'('d cLlniaJ nerves resulting in .lcute onset of 228 right ocular ophthalmoplegia. It was felt, in addition, that the clot was probably now stable and should afford adequate protection against rupture, obviating surgical treatment. Journal of Clinical Neuro-ophtholmolgy References 1. Newton, T.H., and Potts, D.G.: Radiology of skull and brain. In Aneurysms, J.M. Allcock, Ed. c.Y. Mosby, St. louis, 1974, p. 2451. 2. Barr, H.W.K., Blackwood, W., and Meadows, 5.1'.: Intracavernous carotid aneurysms, a c1inicdl-p.lthological report. Brdin 94: 607-b22, 1971. 3. Post, j., Glaser, J.5., dnd Trobe, J.D.: The r.:ldiographic recognition of two clinically elusive m.1SS lesions of the cavernous sinus: Meningiomds dnd aneurysms. Neurorildio/ogy 16: 499-603, 1978. September 1981 R.:Ipport, Murtagh 4. Trobe, j., Glaser, ).5., and Post, J.M.: Meningiomas and aneurysms of the cavernous sinus. Arch. Ophthil/ mol. 96: 457-467, 1978. 5. Post, ).M., Glaser, ).5., and Trobe, J.D.: The radiogr.: lphic diagnosis of Cdvernous meningiomds and dneurysms with a review of the neurovascular anatomy of the Cdvernous sinus. eRC Crit. Rev. Diagn. Imaging 1-33, 1979. Write for reprints to: F. Reed Murtagh, M.D., Division of Neuroradiology, Tampa General Hospital, Tampa, Florida 33606. 229 |
