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Show ]. C1in. Neuro-ophthalmol. 3: 277-281, 1983. Neuroradiological Clinical Pathological Correlations Sixth Nerve Ophthalmoplegia Secondary to a Cavernous Sinus Lesion JOSEPH S. GURINSKY, M.D. ROBERT M. QUENCER, M.D. M. JUDITH DONOVAN POST, M.D. Case History A 60-year-old female presented with as-year history of a sixth nerve paralysis. Outside serial computed tomograms (CT) performed prior to the present workup were interpreted as normal and the patient's left VI paralysis was interpreted as probably secondary to her mild diabetes. Two years prior to the present evaluation, the patient underwent palliative extraocular muscle correction (Jensen's procedure), but postoperatively her lateral diplopia persisted. She then slowly developed numbness and paresthesias in the left VI nerve distribution and on physical examination she was noted to have a diminished left corneal reflex. Plain skull films and tomograms were unremarkable. On coronal CT there was a homogeneously enhancing mass bulging the lateral wall of the left cavernous sinus (Fig. 1). Cerebral angiography was then performed (Figs. 2a and 2b). Discussion - Since our patient suffered primarily from pathology involving the fifth and sixth cranial nerves, involvement of the cavernous sinus was suspected. Therefore, the anatomy relevant to these structures will be discussed. Figure 3 is a diagram of a coronal section through the cavernous sinus and will serve as a guide for the following discussion. From the Department of Radiology, University of Miami School of Medicine, Miami, Florida. December 1983 The cavernous sinus is bounded by dura laterally and superiorly. Venous tributaries to the cavernous sinus enter anteriorly and the sinus drains posteriorly. Specifically the cavernous sinus communicates anteriorly with the superior and inferior ophthalmic veins, the central retinal vein, the middle and inferior cerebral veins, and the middle meningeal veins. Posteriorly it drains into the superior and inferior petrosal sinuses. Inferiorly it drains into the pterygoid plexus. The right and left cavernous sinuses communicate via anterior and posterior venous channels. The normal cavernous sinus appears as an area of increased attenuation lateral to the sella turcica on enhanced coronal and axial CT views. The cavernous sinus is bounded superiorly by both clinoids, posteriorly by the dorsum sella, anteriorly by the superior orbital fissure, inferiorly by the base of the skull, and medially by the sphenoid bone and pituitary gland. Since the lateral sinus wall is strictly lined by dura it is distensible; therefore, it can serve as a sensitive indicator of disease particularly on coronal CT. The normal lateral walls are straight or slightly concave and should be bilaterally symmetrical. With the exception of the neurovascular structures described below, no focal area of inhomogeneity should be present within the cavernous sinus. The cavernous portion of the internal carotid artery, the sympathetic carotid plexus, the oculomotor nerve (1II), the trochlear nerve (IV), the abducens nerve (VI), and the ophthalmic division of the trigeminal nerve (V Jl are contained within the cavernous sinus. The internal carotid artery enters the cavernous sinus posteriorly and inferiorly; as it courses within the sinus it forms an "S" in the sagittal plane. The 277 Sixth Nerve Ophthalmoplegia Figure 1. Coronal CT scan at the level of the cavernous sinus, showing a smooth homogeneously enhancing mass bulging the left wall (arrow). artery may be in contact with the pituitary gland or may lie as far as 2.3 mm lateral to this structure. I On CT scans the internal carotid artery cannot normally be separated from the cavernous sinus because they are of equal density. The oculomotor nerve enters the cavernous sinus slightly anterior and lateral to the dorsum. It then runs in the superolateral margin of the cavernous sinus between the two dural sheets, finally entering the orbit through the superior orbital fissure. Therefore, it appears on postcontrast CT as an ovoid-filling defect within the superior portion of the cavernous sinus. The trochlear nerve enters the cavernous sinus posterolateral to the posterior clinoid process. It lies within the lateral wall of the cavernous sinus inferolateral to the oculomotor nerve. Throughout its intracavernous course, the trochlear nerve is invested by dura. It enters the superior orbital fissure in a position superior to that of the oculomotor nerve. Coronal CT cannot usually separate the trochlear from the oculomotor nerve. The abducens nerve originates at the lower border of the pons. As it ascends along the clivus it is enclosed in dura. The sixth nerve enters Dorello's canal, passes beneath the petroclinoid ligament, (AI Figure 2a. Arterial phase of left interIMI carotid angiogram, lateral view. The precavernous and proximal cavernous portions are encased. There is hypertrophy of the meningohypophyseal trunk (single arrow) and a vascular blush which arises from these vessels (arrowheads). Journal of Clinical Neuro-ophthalmology Gurinsky, Quencer, Post Figure 2b. Arterial phase of left internal carotid angiogram (Waters projection) shows encasement (arrows) of the precavernous and proximal cavernous carotid artery. There is faint visualization of tumor vessels surrounding the encased vessel. and pierces the dura of the cavernous sinus approximately 2 mm below the posterior clinoid. Within the sinus it lies in proximity to the lateral aspect of the cavernous carotid artery. It enters the superior orbital fissure between nerves III and IV. The abducens nerve may be visualized by coronal CT lateral to the position of the carotid artery (Fig. 3). The ophthalmic division of the trigeminal nerve (VI) passes posteriorly through the superior orbital fissure and enters the lateral wall of the cavernous sinus. After running laterally and inferiorly it exists posteriorly to reach the gasserian ganglion. VI lies within the cavernous sinus in a plane inferior to I III, IV, and VI and it is invested by dura. By CT, VI December 1983 is visualized as a large OVOid-filling defect in the inferolateral margin of the cavernous sinus. In one large series,2 in which the etiology of 275 cases of VI nerve paralysis could be determined, the following were obtained: neoplasms (159), head trauma (55), vascular disease (46), and intracranial aneurysms (15). Our patient had no history of head trauma, and in addition, the lack of a significantly worsening clinical picture over a 5-year period of time is against an intra-axial (i.e., brain stem) neoplasm. The progressive involvement of VI is against a vascular etiology. A lesion within the cavernous sinus could explain this patient's initially isolated sixth nerve ophthalmoplegia and CT findings. Intracavernous 279 Sixth Nerve Ophthalmoplegia Figure 3. Artist's diagram of a coronal section through the cavernous sinus. (Adapted from Post, M.JD., Glaser, J.5., and Trobe JD.: Radiographic diagnosis of cavernous meningiomas and aneurysms with a review of the neurovascular anatomy of the cavernous sinus. CRC Crit. Rev. Diagn. Imag. 1-33; 28, 1979. Medical Illustrator, Leona M. Allison, MD.) mass lesions are most frequently vascular or neoplastic in origin. The majority of intracavernous vascular masses are aneurysms. Neoplasms which may affect the cavernous sinus include meningiomas, neuromas (predominantly of Vd, metastases, and tumors extending into the cavernous sinus from adjacent structures. An inflammatory process such as a mucocele may also compress the cavernous sinus. Neuromas involving the cavernous sinus are comparatively rare, and when they involve either the gasserian ganglion or the Vj nerve root, they produce early trigeminal symptoms. In addition, gasserian neuromas usually produce destruction of the sphenoid wing or lateral wall of the sphenoid sinus,:J a finding not present in our case. Metastatic disease from an unknown primary is unlikely in view of the prolonged clinical course without painful symptomatology. The absence of adjacent bony changes mitigates against extension of tumor or inflammatory process from the nasopharynx, sphenoid sinus, or sella turcica. In our patient, the differential diagnosis rests between an aneurysm of the cavernous carotid and an intracavernous meningioma. Cerebral angiography excluded an aneurysm. It demonstrated narrowing (i.e., encasement) of the precavernous and proximal cavernous left internal carotid artery (Figs. 2a and 2b) with enlargement 280 of the meningohypophyseal trunk and a homogeneous tumor blush in the region posterior to the precavernous carotid (Figs. 2a and 2b). Although surgery has not been performed at the time of writing, these findings are most consistent with a diagnosis of cavernous sinus meningioma. Cavernous sinus meningiomas are classically seen in middle-aged female patients who present with slowly progressive unilateral painless ophthalmoplegia. The isolated VI nerve findings in this case are uncommon. Findings on plain films may include hyperostosis, tumoral calcifications, soft tissue density within the sphenoid sinus, unilateral sphenoid sinus erosion, anterior clinoid erosion, an abnormal sellar configuration, and destruction of the sellar floor. However, these are late radiographic features. CT examination may show all these findings, but in addition has the advantage of showing an enhancing soft tissue mass bulging the lateral wall of the cavernous sinus early in the course of the disease (Fig. 1).4 When meningiomas in this region are small, the detection of contrast enhancement is difficult because the mass is located in a highly vascular structure (the cavernouS sinus). Nevertheless, bulging of the lateral wall can be used as a sensitive sign of an intracavemous mass. When arteriography of a cavernous sinus meningioma is performed, abnormal vessels from both Journal of Clinical Neuro-ophthalmology the internal and external carotid arteries may be seen. An enlarged meningohypophyseal trunk and an enlarged artery to the inferior cavernous sinus arising from the internal carotid are the most commonly involved vessels. Supply from the external carotid via the middle meningeal artery, accessory meningeal artery, and artery of the foramen rotundum may also be seen, particularly in larger meningiomas. A homogeneous tumor blush is seen in the capillary and venous phases. The classical angiographic features of a cavernous meningioma are seen in Figure 2. References 1. Kline, C. B., Acher, J. D., Post, M. J. D, and Vitek, J. J.: The cavernous sinus: A computed tomographic December 1983 Gurinsky, Quencer, Post study. A.].N.R. 2: 299-305, 1981. 2. Rucker, C. W.: The causes of paralysis of the third, fourth and sixth cranial nerves. Am. ]. Ophthalmol. 61: 1293-1298, 1966. 3. Schubiger, 0., Valavanis, 0., Hayek, J., and Dabri, K.: Neuroma of the cavernous sinus. Surg. Neural. 13: 313-316, 1980. 4. Post, M. J. D., Glaser, J. S., and Trobe, J. D.: The radiographic recognition of two clinically elusive mass lesions of the cavernous sinus: Meningiomas and aneurysms. Neuraradiology 16: 499-503, 1978. Write for reprints to: Robert M. Quencer, M.D., Department of Radiology (R-130), University of Miami School of Medicine, P.O. Box 016960, Miami, Florida 33101. |
