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Show J. Clin. Neuro-ophthalmol. 4: 247-250,1984. Papilledema and Dural Sinus Obstruction MICHAEL X. REPKA, M.D. NEIL R. MILLER, M.D. Abstract We present two cases of meningioma obstructing the posterior sagittal sinus, producing elevated intracranial pressure and papilledema by impairing cerebral venous drainage. In both patients, this mechanism was not recognized preoperatively and resulted in optic atrophy and significant visual loss. Introduction An intracranial mass can produce elevated cerebrospinal fluid (CSF) pressure and papilledema in at least three ways. 1) The most common mechanism is a direct mass effect, often from a posterior fossa lesion. 2) The second most commonly encountered mechanism is blockage of the ventricular system by the mass. 3) Much less commonly, elevation of cerebrospinal fluid pressure is produced by obstruction of cerebral venous outflow.~-4 We present two patients in whom the existence of this last mechanism was not suspected. Instead, initial therapy was directed at resection of the lesion without measures to improve venous drainage. The delay in reducing intracranial pressure resulted in irreversible visual loss. Case Reports Case 1 A 45-year-old woman presented to the Johns Hopkins Hospital with a 6-month history of light headedness, binocular horizontal diplopia, and blurred vision. Ophthalmologic examination revealed visual acuities of 20/20 in the right eye and 20/15 in the left eye. The patient could identify nine out of 10 Hardy-Rand-Rittler (HR- R) pseudoisochromatic color plates with the right eye and six out of 10 with the left eye. Visual fields showed a relative binasal defect in both eyes. Bilateral abduction weakness was present, and there was bilateral chronic papilledema. From the Departments of Ophthalmologv (MXR, NRM), Neurosurgery (NRM), and Neurology (NRM), Johns Hopkins Universitv, School of Medicint'. Baltimore. Maryland. December 1984 Computerized tomographic (CT) scanning on admission demonstrated a small enhancing lesion involving the posterior superior falx (Fig. la), with normal ventricular size (Fig. Ib). Arteriography showed a relatively avascular mass obstructing the posterior superior sagittal sinus (Fig. 2). Craniotomy was performed, at which time the lesion was found to be a meningioma. The tumor was completely resected, but no attempt was made to reconstruct the posterior superior sagittal sinus which had been infiltrated and occluded by the tumor. No shunting procedure was performed. One week postoperatively, the patient's visual acuity and papilledema were unchanged, but color acuity had decreased to 4.5 out of 10 with the right eye and 3.5 out of 10 with the left eye. The patient was subsequently lost to follow-up for 8 weeks, during which time she noted progressive loss of visual acuity. When she was reexamined, acuity was 20/40 in the right eye and 20/50 in the left eye, and she was unable to identify any of the color plates. Perimetry demonstrated further loss of both nasal fields. The disc swelling was unchanged from the preoperative evaluation. A CT scan was normal; however, cerebrospinal fluid pressure was 240 mm water. There was normal glucose and protein content and no cells. The patient was treated with furosemide and dexamethasone with reduction in CSF pressure to 200 mm water over 3 days. After 8 additional weeks of medical therapy, the disc swelling finally resolved, and there was an improvement in both visual acuity and visual fields, but without improvement in color vision. Both discs became pale, and there was significant reduction in visible nerve fiber layer in both eyes. Medical therapy was gradually stopped, ~nd there was no return of disc swelling. Case 2 A 50-year-old man presented with a I-month history of five episodes of transient visual obscurations. The obscurations involved both eyes and lasted 3-4 seconds. They were unassociated with systemic or neurologic symptoms; however, 247 Dural Sinus Obstruction {al Figures la and lb. CT scans of case normal size (b). tttl A small enhancing mass involves the posterior superior falx (al. The ventricles are of 248 Figure 2. Arteriogram of case 1. An avascular mass is seen obstructing the posterior superior sagittal sinus. Journal of Clinical Neuro-ophthalmology Repka, Miller e,l) Figures 311 and 3b. CT scans of case 2. A Idt cerebl'lIopontine angle tumllr (II) and a small left para,agittall1ccipital mass (II) are seen. the patient had long-standing diminished hearing on the left side. Visual acuity was 20/40 in the right eye and 20/20 in the left eye, and the patient was able to identify all the H-R-R pseudoisochromatic color plates with each eye. There was a trace afferent pupillary defect on the right, and both visual fields had enlarged blind spots. Motility examination demonstrated mild deficiency of right abduction. Ophthalmoscopy revealed chronic papilledema. CT scan demonstrated two enhancing masses: a left cerebellopontine angle (CPA) lesion displacing the fourth ventricle (Fig. 3a) and a small left parasagittal occipital lobe lesion with surrounding lucency (Fig. 3b). The ventricular system was of normal size. Arteriography showed vascular displacement by both masses as well as obstruction of the posterior superior sagittal sinus with minimal collateral vascularization (Fig. 4). It was elected to remove the parasagittal mass as the first procedure. At surgery, a small meningioma was found that was infiltrating and obstructing the posterior portion of the superior sagittal sinus. The tumor was completely removed, but the sinus was not reconstructed, nor was a shunt procedure performed. One week postoperatively, the patient's visual acuity was 20/60 in the right eye and 20/40 in the left eye, and he had a December 1984 Figure 4. Arteriogram llf case 2. An aVilscular mass is obstructing the posterior superior sagittal sinus. marked right afferent defect. The left visual field was unchanged, but there now was only a temporal island of vision remaining in the right eye. The patient continued to experience multiple 249 Dural Sinus Obstruction transient obscurations of vision in both eyes at an increasing rate. Papilledema remained unchanged. CT continued to demonstrate a normal ventricular system. The patient was treated with acetazolamide 250 mg four times a day. Four weeks later, a 90% resection of a left acoustic neuroma was performed. Again no shunt procedure was performed. Following the second procedure, the patient's visual acuity became no light perception in the right eye and 1/400 in the left eye. Bilateral abduction deficits were present. Over the next 4 weeks, the patient's disc swelling and abduction deficits resolved, but there was no improvement in either visual acuity or visual field. Discussion In both of the patients described above, intracranial lesions produced papilledema, not solely by a mass effect, but by obstructing venous outflow and thereby reducing CSF absorption. The first patient had a small meningioma compressing the posterior superior sagittal sinus and obstructing normal cerebral venous drainage. This dural sinus was further disrupted surgically and was not repaired. The intracranial pressure took 17 weeks to normalize, a time course compatible with venous collateral formation and reestablishment of CSF absorption. This protracted course resulted in substantial loss of optic nerve function as demonstrated by decreased color vision and the development of further visual field defects. The second patient had two intracranial masses, a small falx meningioma infiltrating the posterior superior sagittal sinus and an acoustic neuroma. Neither tumor was thought to be large enough to produce any significant obstruction of the ventricular system. Despite removal of both masses, this patient continued to have elevated intracranial pressure for 10 weeks, resulting in profound irreversible visual loss. As in the first case, the period of time required to normalize the intracranial pressure after resection of the occipital meningioma was not compatible with relief of a mass effect, but followed the time course of restoration of normal cerebral venous flow by collateral formation. Impaired venous drainage of the brain is a welldocumented cause of papilledema. First recognized in 1933 by Byers and Haas" in a patient with dural thrombosis, the syndrome may be produced by radical neck dissection,';h trauma/ and thrombophlebitis of a dural sinus, often from a contiguous otitic process.~ Marr and ChambersQ reported two patients with parasagittal meningiomas that infiltrated and obstructed the posterior superior dural sinus producing papilledema and, eventually, optic atrophy. Both of these patients required shunt procedures because of persistent 250 elevation of intracranial pressure and progressive destruction of their optic nerves. Subsequently, there was apparent stabilization of their ocular course. In the two cases we have described, significant visual function was lost because of delayed recognition of the primary cause of elevated intracranial pressure. We suggest that if venous outflow obstruction is considered to be a contributing factor in the elevation of the CSF pressure, or if the dural drainage system is found to be disrupted at surgery, the patient should be treated for the pseudotumor cerebri syndrome. This may involve postoperative medical management, multiple lumbar punctures, or placement of a CSF shunt. If the papilledema is severe, consideration should be given to reconstruction of the dural sinus or performance of a lumbo-peritoneal shunt at the time of the tumor resection. To delay these relatively benign procedures can only result in progression of optic nerve dysfunction until sufficient collaterals have formed, usually after much vision is irreversibly lost. References 1. Miller, N.R.: Walsh and HOl/t's Clinical NeuroOplltllalllloloy (4th ed.). Willia'ms & Wilkins, Baltimore, 1982, pp. 175-211. 2. Petrohelos, M.A., and Henderson, J.W.: The ocular findings of intracranial tumor. Trans. Am. Acad. Ophthalmol. 55: 89-98, 1950. 3. Bvers, R.K., and Haas, C.M.: Thrombosis of the di.lfal venous sinuses in infancy and in childhood. Am. f. Dis. Gild 45: 1161-1183, 1933. 4. Marr, W.G., and Chambers, J.W.: Pseudotumor cerebri syndrome following unilateral radical neck dissection. Am. f. Ophthalmol. 51: 605-609, 1961. 5. Fitz-Hugh, G.5., Robins, R.B., Craddock, W.O.: Increased intracranial pressure complicating unilateral neck dissection. LarY'lgoscopc 76: 893-906, 1966. 6. Tobin, H.A.: Increased cerebrospinal fluid pressure following unilateral radical neck dissection. Laryngoscope 82: 817-820,1971. 7. Martin, J.P.: Signs of obstruction of the superior longitudinal sinus following closed head injuries (traumatic hydrocephalus). Br. Mcd. J. 2: 467-470, 1955 8. Symonds, c.P.: Hydrocephalic and focal cerebral symptoms in relation to thrombophlebitis of the dural sinuses and cerebral veins. Brain 60: 531550,1937. 9. Marr, W.G., and Chambers, J.W.: Occlusion of the cerebral dural sinuses. Am. f. Ophthalmol. 61: 4549,1966. Acknowledgment This work was supported in part by a National Eye Institute Training Grant 2T32EY07047 (Dr. Repka). Journal of Clinical Neuro-ophthalmology |
