Journal of Neuro-Ophthalmology, September 1982, Volume 2, Issue 3

Optic disc changes with intracranial subarachnoid cysts.

We have recently encountered two patients who presented with ophthalmoscopically unusual optic disc changes, and who were found to have intracranial subarachnoid cysts. The discs appeared chronically swollen, had microtelangiectatic vessels on the surface and leaked fluorescein. This report documents unusual swollen discs in patients with no clinical evidence of increased intracranial pressure yet who are found to have intracranial subarachoid cysts by computed tomography.

]. C/in. Neuro-ophth.l/nwl. 2: 183-IQ2, IQ82. Optic Disc Changes with Intracranial Subarachnoid Cysts* HOWARD CONN, M.D. RICHARD R. TENZEL, M.D. J. LAWTON SMITH, M.D. Abstract We have recently encountered two patients who pre­sented with ophthalmoscopically unusual optic disc changes, and who were found to have intracranial subarachnoid cysts. The discs appeared chronically swollen, had microtelangiectatic vessels on the surface iUld leaked fluorescein. This report documents unu­sual swollen discs in patients with no clinical evi­dence of increased intracranial pressure yet who are found to have intracranial subarachoid cysts by com­puted tomography. Case Reports Patient 1 A 52-year-old man was first seen on June 23, 1977. He began to note painless, progressive visual loss of the left eye at age 42, and in 1967 his visual acuity was 20/25+ in the right eye and 20/200 in the left eye. The right eye first became involved in 1972. At that time his visual acuity was 20/200 in both eyes, and the left eye remained at the same level thereafter. A 2-week course of oral steroids at age 51 did not improve the visual function. He has had occasional headaches and has had a rup­tured left lumbar sacral disc. He had a history of tachycardia controlled with digoxin, but was in good health otherwise. Neuro-ophthalmologic examination on June 23, 1977, revealed a visual acuity of 33/200 in the right eye and 30/200 in the left eye. Near visual acuity was correctable in both eyes to J-l at 6 in. with a +5.50 sphere. The pupils were equal in size and reacted 2-3+ to light. There was no afferent pu­pillary disturbance. Extraocular movements were normal. Perimetry revealed bilateral enlargement of the blind spots and cecocentral scotomas with From the Bascom Palmer Eye Institute, Department of Oph­thalmology, University of Miami School of Medicine, Miami, flOrida. • Presented at the 18th Annual Residents' Day meeting of the Bascom Palmer Eye Institute, Miami, Florida, June 20, 1982. September 1982 full peripheral fields. Exophthalmometry was 18 in both eyes at a base of 100. Ophthalmoscopy revealed an unusual abnor­mality of the discs. In the right eye (Fig. 1a), the nerve head was slightly elevated and many small telangiectatic vessels crossed the temporal side. A few dilated vessels were seen on the upper nasal margin. The disc was of normal color and had a small cup. Fine glial-like balls lay on the temporal surface of the disc, and a small hemorrhage was seen at 10:30. The disc venules were full without spontaneous venous pulsations. The retina adja­cent to the temporal margin was elevated with clear subretinal fluid. A partial macular star figure ex­tended towards the fovea. The fundus was symmetrical in the left eye. The disc (Fig. 1b) was swollen, and although the disc venules did not appear notably distended, it re­quired considerable pressure on the lids to make the veins collapse. The left macula had a less apparent star figure, and the fovea was normal. The peripheral fundus was normal in both eyes. Fluorescein angiogram (Figs. 2a and 2b) revealed late staining of the discs. The initial impression was that the patient had bilateral chronic optic nerve disease, etiology un­known, characterized by staining of the discs with fluorescein, small telangiectatic vessels on the tem­poral discs and a partial star figure in the macula. Atypical papilledema, juxtapapillary vascular hamartoma, circumpapillary telangiectatic micro­angiopathy, unusual chronic optic neuritis, and atypical Leber's optic nerve disease were consid­ered in the differential diagnosis. A computed tomographic scan of the brain and orbits (Figs. 3a and 3b) was made on July 10, 1979. This revealed a large, well-circumscribed sub­arachnoid cyst that filled approximately 25% of the cranial volume in the right middle cranial fossa anteriorly, and it extended superiorly into the fron­totemporal region. The absorption values were compatible with cerebrospinal fluid. This cyst communicated with a contralateral small left mid­dle cranial fossa cyst across the midline at the level of the suprasellar cistern. The cyst was clearly 183 Intracranial Subarachnoid Cysts Figure lao Case 1. Right optic disc on July 10, 1979. The disc is somewhat elevated and white arrowheads show the margin of the swelling. The small black arrowheads point to small telangiectatic vessels on the temporal side. Hgure Ib, Lase I. Lett optiC disc. 1his disc is also swollen and black arrowheads point to small telangiectatic vessels. Journal of Clinical Neuro-ophthalmology Figure 2~. Case 1. Fluorescein angiogram of right eye, showing delayed staining of the right disc. Figure 2b. Case 1. Fluorescein angiogram showing staining of left optic nerve head. September 1982 Conn, Tenzel, Smith Fjgure 3a. Computed tomographic brain scan, axial view. of case 1, on August 10, 1981 (after contrast enhancement). Large extra-axial subarachnoid cyst in right middle fossa (three white arrowheads delineate the cyst). The cyst communicates with a small left middle fossa cranial cyst across the midline at level of suprasellar cistern. (Single white arrowhead is in the left middle fossa cyst.) Figure 3b. Computed tomographic brain scan, case 1, coronal view. The subarachnoid cyst is delineated by arrows-note the much greater size of cyst in right middle fossa as compared to the smaller cyst on left side (continuous across midline). Frontal horns of the ventricles are asymmetric, with slight flattening of left frontal horn by the cyst. 185 Intr.1Cranial Subarachnoid Cysts extra-axial with posterior displacement of the branches of the middle cerebral artery. The right lesion produced a shift of the septum pellucidum to the left. There was a mass effect upon the inferior portion of the third ventricle and right internal carotid artery near the internal carotid artery bifurcation. There was a widened right syl­vian fissure and compression of the right lateral ventricle in the region of the body and frontal horn. The frontal sinuses were markedly enlarged (Figs. 4-6). The orbital views were of good quality and revealed a normal appearance to the orbital optic nerves. The patient was followed carefully from 1977 to 1981 without apparent change in visual function or ophthalmoscopic appearance. Because of the per­sistence of the bilateral chronic optic disc edema, the patient was admitted to the Bascom Palmer Eye Institute/Anne Bates Leach Eye Hospital on August 11, 1981. His blood pressure was 134/80. A neu­rological examination revealed absent left knee jerk and mild sensory loss over the anteromedial aspect of the left lower leg, consistent with the history of a herniated L-4 lumbar sacral disc on the left side. The remainder of the examination was unremarkable. Skull roentgenograms demonstrated marked de­mineralization of the dorsum sellae and faint cal­cification of the carotid siphon. Plain and enhanced computed tomography of the orbits and brain were performed. The intracranial subarachnoid cyst was unchanged in appearance from the study 2 years earlier. There were no orbital abnormalities, and specifically, dilation of the optic nerve sheaths was not apparent. A-scan ultrasound suggested bilat­eral optic nerve sheath distension due to increased fluid between the sheath surfaces and optic nerves. Maximal width of the optic nerve patterns, meas­ured from the inner surface of the arachnoid sheath were 7.0 mm on the right and 6.9 mm on the left. Measurements were performed with the standard­ized A-scan (Kretztechnik nooMA). Contact B­scan examination using the Osuscan 400M also suggested bilateral optic nerve sheath distension. The impression was that the patient had bilateral temporal lobe subarachnoid cysts and bilateral chronic papilledema, probably secondary to the optic nerve sheath cysts. We elected to perform right optic nerve de­compression on August 12, 1981, because of the intractible persistence of the papilledema. A tran­sconjunctival approach was selected. After con­junctival peritomy, the medial rectus was detached, and a traction suture was placed through the medial rectus stump. The optic nerve was exposed. The nerve sheath was distended. Upon compressing the nerve sheath with a cotton-tipped applicator, the sheath flattened at the site and distended adjacent to the site of compression, suggesting that fluid lay beneath the nerve sheath. A 2 X 3 mm opening was made in the nerve sheath nasally. The histo­pathologic examination of the excised tissue re­vealed collagenous stroma containing elongated fibroblasts, vascular channels, and glial cells con­sistent with a normal optic nerve sheath. On the first postoperative day, A-scan and B­scan ultra sound examinations revealed that there was less distension of the right optic nerve sheath. A-scan measurements were 4.0 mm right eye (3.1 mm less that the preoperative evaluation) and 7.4 mm left eye (0.5 mm more than measured preop­eratively). Examination on February 9, 1982, 6 months postoperatively, revealed a visual acuity of 27/200 in the right eye and 35/200 in the left eye. The appearance of the discs remained unchanged. Patient 2 A 40-year-old man was first examined on No­vember 21, 1981. He noted bifrontal and bitem­poral headaches from 9 to 10 months prior to examination, which were relieved by the use of reading glasses. Eight to 10 weeks prior to exami­nation, he noted metamorphopsia and a positive scotoma in the right eye. Specifically, he observed that vertical parallel lines appeared to bow, diverg­ing at their ends and converging centrally. Occa­sionally, a gray spot appeared in his central vision. He had no other visual or neurologic complaints. Neuro-ophthalmologic examination revealed a visual acuity of 20/20-2 slowly in the right eye and 20/15 + 3 rapidly in the left eye. Near visual acuity was correctable to J-l slowly right and J-l rapidly in the left eye at 15 in. with a +1.50 sphere. The pupils were equal in size, reacted crisply to light, but there was a definite afferent pupillary response on the right. Extraocular movements were nonnal. Perimetry revealed a subtle but definite cecocentral scotoma in the right eye to 5/1000 white projection light and bilaterally intact peripheral fields. Color vision testing with the AO pseudoisochromatic color plates elicted correct responses: 11.5/15 right eye and 14/15 left eye. He reported a nonnal Amsler grid pattern with the left eye and some bowing on the temporal and inferior aspects with the right eye. This aberration was not abolished with pinhole or refractive spectacles. The right optic disc (Fig. 701) had some temporal pallor. The nasal side was sharp. There was no elevation nor increase in cupping. The disc venules were of normal size,. but pressure on the lids was needed to make the veins pulsate. There were a few white dots and drusen in the fovea (Fig. 6) and a slight alteration of the foveal reflex. The capillaries on the upper temporal margin of the fovea were slightly tortuous. The left disc (Fig. 7b) had a sharp outline, nonnal color, and small cup. There were abnormal telangiectatic vessels on the temporal side of the disc. The disc venules and fovea were Journal of Clinical Neuro-ophthalmology Conn, Tenzel, Smith Figure 4. Case 1. Orbital computed tomographic scan, (August 10, 1981). Orbital optic nerves appear normal on this scan. Margin of cyst on left side delineated intracranially by white arrowhead. Figure 5. Case 1. Axial cut, enhanced, of CT scan, showing enlarged frontal sinuses (open white arrowheads). Solid white arrowhead shows the subarachnoid cyst. Note slightly protein­aceous appearance of cyst contents here. September 1982 Figure 6. Case 1. CT scan at higher cut shows upper margin of the intracranial subarachnoid cyst. 187 Intr.lCr.mial Subarachnoid Cysts Figure 7... C.1Se 2. Right optic disc. NllVember 17. )081. S,'me tempor~1 p~II,>r w~s ~pparent dS comp.>red t" left optic nerve. Figure 7b. C~se 2. left optic disc l'n Novt"mber 17. (081. Slight blurring of ndsdl miJrgin is seen. Abnorm,,1 smdll tel.1ngit"ct,l!ic vessl,ls on tt"mpor.,1 sidt" ,Ut" dt"linedted by sm,,11 bl"ck Jrrowhe.,ds. normal. Retroillumination revealed a small pig­ment epithelial window defect on the upper nasal side of the left fovea. There was slight tortuosity of the capillary net on the temporal side of the fovea. Peripheral fundi of both eyes were normal. The initial impression was that the patient had right-sided, chronic optic nerve disease, etiology unknown, characterized by an afferent pupillary defect, reduced color vision, a cecocentral scotoma, and optic disc pallor of the right eye. The left eye had disc telangiectasia. Since the right eye symptoms of metamorphop­sia and positive scotoma were so characteristic of retinomacular disease, a fluorescein angiogram was Journal of Clinical Neuro-ophthalmology performed and showed no significant evidence of disease at the foveas. ERG and EOG studies were normal. The same differential diagnosis clS de­scribed in case 1 was considered. A computed tomorgraphic scan of the brclin WclS made on November 16, 1981. This revealed a sub­arachnoid cyst at the right subtemporal region which extended up through the sellcl (Figs. 8-11). Metrizamide was given by spinal tclP injection on November 19, 1981. The subarclchnoid cyst filled with dye. An arteriogram done on November 17, 1981, showed no other clbnormcllities. The pcltient was seen again on May 13, 1982, clnd his eXclmi­nation was unchanged. Discussion Arachnoidal cysts are fluid-filled cavities lined by neuroepithelial cells. They may occur anywhere in the neuroaxis where there are arachnoid me­ninges or cell rests. Their origin may be congenital or secondary to trauma or inflammation. Most are asymptomatic,1 however, they may become symp­tomatic through tumor-like mass effects on sur­rounding structures.2 Benes et al. have contributed a major review of their ocular manifestations.3 They reviewed 193 reported cases from the litera­ture and presented four new cases. The cysts were classified as congenital, post-traumatic, and postin­flammatory, with approximately equal frequencies. Figun 8. Case 2. Computed tomographic brain scan, enhanced, axia.I view (November 16, 1981), reveals a subarachnoid cyst at the right subtemporal region which extends up through the sella. White arrowhead delineates cyst margin. September 1982 Conn, Tenzel, Smith Figure 9. Case 2. Another cut of CT scan showing cyst extending across the midline. Figure 10. Computed tomographic scan of orbits, case 2 (No­vember 16, 1981), reveals normal appearing orbital optic nerves. lntracrnial cyst margin is shown by white arrowhead on the patient's right. Rarely, tumor-associated arachnoid cysts were found with optic and pontine gliomas and menin­giomas. Half of the patients were diagnosed before the age of 15 and had symptoms of hydrocephalus and psychomotor or growth retardation. Signs and symptoms in adults varied with the location of the cyst. Seventy percent of the cysts occurred in the basal portions of the cranial vault, the temporal 189 Intr'lcranidl Subarachnoid Cysts Figure 11. Computed tomographic brain scan, coronal view, case 2. Intracranial subarachnoid cyst in right subtemporal region (white arrowhead). Note asymmetry of frontal horns (compare with case 1 in Fig. 3b). fossa, posterior fossa, and parasellar region. The remaining 30% occurred in the uppermost cranial vault, or were 50 extensive that they filled an entire hemisphere. Over 50% of the adult patients com­plained chiefly of headaches, 30%-40% had blurred vision and 15% had diplopia. Eighty-three percent of the patients examined ophthalmoscopically had ocular abnormalities. These included reduction in visual acuity, abnormal visual fields, ocular motil­ity disturbances and, rarely, opticociliary shunt vessels and proptosis. Papilledema was seen with cysts in all locations. Optic atrophy was present in patients with optic tract lesions and in some pa­tients with optic nerve, parasellar, temporal, and cerebellar lesions. Most of the patients had other neurological signs which aided in localizing the lesions. However, cysts located in the temporal and frontal lobes did not always have other neurologi­cal signs which pointed to their locations. One of the four new cases that Benes presented was a 74­year- old woman with a left frontotemporal intra­cerebral mass who had only bilateral visual field 1055 and optic atrophy. More recent reports con­firm the high frequency of optic atrophy and disc swelling in patients with arachnoid cystS.4-IH Krohel Jnd Hepler!!' have reported the unusual occurrence of ipsilateral glaucoma, glaucomatous opti~ atro­phy, and an optic nerve sheath cyst contiguous with a left temporal fossa arachnoidal cyst.. . The two cases presented had disc telangIectasIa. ]uxtapapillary telangiectasia of retinal vesse!s ~ith optic atrophy has bee~ noted a~ characten~tI~ ~f Leber's optic atrophy.2 Cases WIth a slow, inSIdI­ous onset21 and also atypical acute onsetZO • 22 have been reported. Heckenlively et al. 23 have recently reported temporal disc atrophy and telangiectasia of disc vessels in patients with cone-rod dysfunc­tion. It was suggested that the telangiectasia may represent a localized vascular response to a degen­erative process occurring in the nerve fiber layers. The first case presented had bilaterally dilated optic nerve sheaths as documented by ultrasound. This may have been secondary to a nonspecific mass effect of the intracranial cyst producing in­creased intracranial pressure. Alternatively, the pa­tient may have had bilateral arachnoidal cysts of the optic nerves isolated from or in communication with the intracranial cyst. Arachnoidal cysts of the optic nerve have been reported in association with gliomas,24 neurofibromas,25 and as isolated find­ings. 26-2~ Two cases have been described of a uni­lateral optic nerve cyst associated with an intracra­nial arachnoidal cyst. The first patient had a por­encephalic cyst and a saccular enlargement of the optic nerve sheath adjacent to the globe. Histo­pathologic examination of the dilated optic nerve sheath showed meningoendothelial cell prolifera­tion of the arachnoid.26 The second report was of an arachnoid cyst of the temporal lobe with an associated cystic orbital lesion adjacent to the optic nerve. 19 Although pathologic confinnation of the optic nerve cyst was not present, ultrasonic exam­ination suggested a cystic lesion. In addition, intra­cranial decompression of the temporal lobe lesion resulted in shrinkage of the orbital lesion, suggest­ing an anatomical connection between the two. The markedly enlarged frontal sinuses in our first case provide evidence that the intracranial arachnoidal cyst developed early in life, since fron­tal sinus enlargement occurs as a compensation for the lack of development of nonnal cerebral tissues. In 1872, deWecker first described incision of the orbital optic nerve sheath for the relief of papille­dema in patients with inoperable but slow-growing brain tumors.:!8 Hayreh29 demonstrated its efficacy experimentally in the primate. Smith et al.30 re­ported the successful treatment of a choked disc due to an optic nerve cyst by making a window in the orbital optic nerve sheath. Optic nerve de­compression has successfully treated patients with papilledema due to many different causes.31 - 33 Op­tic nerve sheath decompression has not produced an improvement in the visual function of the first case. There are at least two possible explanations for this lack of improvement: the nerve sheath Journal of Clinical Neuro-ophthalmology window may have closed due to scarring, and the chronically elevated pressure in the nerve sheath may have produced irreversible optic nerve dam­age. Bilateral chronically swollen discs may be caused by increased cerebrospinal fluid pressure and mimicked by other optic nervehead disorders. Its slow, longstanding temporal profile distinguishes intracranial subarachnoid cysts from other causes of bilaterally chronically swollen discs. Ischemic optic neuropathy and Leber's optic nerve disease are characterized by an abrupt loss of vision in the affected eyes.~'1) The visual loss in the second eye of the patient with Leber's optic nerve disease invariably occurs within 1 year of visual loss in the first eye. Because of the long, stable course of the patient with intracranial subarachnoid cysts, sur­gical intervention does not appear to be urgent. Intracranial subarachnoid cyst must be consid­ered when a patient presents with unilateral or bilateral chronically swollen optic discs of an un­usual appearance with small telangiectatic vessels on the disc. The diagnosis can be promptly made with computed tomography of the brain. References 1. Starkman, S.P., Brown, T.C, and Linell, LA: Cere­bral arachnoid cysts. ]. Neuropathol. Exp. Neurol. 17: 484, 1958. 2. Little, J.R., Gomez, M.R., and MacCarty, CS.: Infra­tentorial arachnoid cysts. ]. Neurosurg. 39: 380, 1973. 3. Benes, S.C, Kansu, T, Savino, P.J., and Schatz, N.J.: Ocular Manifestations of Arachnoid Cysts. In Neuro-Ophthalmology Symposium of the Univer­sity of Miami and the Bascom Palmer Eye Institute, Vol. 10, J.5. Glaser, Ed. CV. Mosby Co., St. Louis, 1980. 4. Gacassi, L, Piazza, G., Gaist, G., and Frank, F.: Arachnoid cysts of the middle cranial fossa: A clin­ical and radiological study of 25 cases treated sur­gically. Surg. Neurol. 14: 211-219,1980. 5. Kuzuhara, M., Shimura, T, Yojima, K., NakaZawa, S., and Honda, K.: Two cases of arachnoid cyst in siblings. No To Hattatsu 2: 309, 1980. 6. Rengachary, 5.5., Watanabe, I., and Brackett, CL Pathogenesis of intracranial arachnoid cyst. Surg. Neurol. 9: 139-144, 1978. 7. Sprung, C, and Mauersberger, W.X.: Value of com­puted tomography for the diagnosis of arachnoid cysts and assessment of surgical treatment. A (Suppl.) Acta Neurol. Chir. (Wien) 28(SuppI.): 619-626, 1979. 8. Spaziante, R., deDivitiis, E., Stella, L., Cappabianca, P., and Donzelli, R.: Benign intrasellar cysts. Surg. Neurol. 15: 274-282, 1981. 9. Menezes, A.H.: Arachnoid cysts in children. Arch. Neurol. 37: 168-172, 1980. 10. Vaquero, J., Carrillo, R., Cabezudo, J.M., Nombela, L., and Bravo, G.: Arachnoid cysts of the posterior fossa. Surg. Neurol. 16: 117-121, 1981. 11. Belloni, G., Cardarelli, M., DiRocco, C, and Rossi, G.F.: Extra-axial subarachnoid cyst of posterior September 1982 Conn, Tenzel, Smith fossa: Clinical diagnostic studies. Acta Neurol. Chir. (Wien) 44: 258, 1978. 12. Bollati, A, Gandolfini, M., Marini, G., Gaini, 5., Giovanelli, M., and Tomei, T: Posterior fossa arach­noidal cysts. Acta Neurol. Chir. (Wien) 44: 259, 1978. 13. Colangelo, M., Vitale, C, Pirrone, R., Daniele, B., Palmieri, A., and Ambrosio,S.: Arachnoidal cysts and enlargement of the cerebrospinal fluid space in the posterior fossa. Acta Neurol. Chir. (Wien) 44: 258-259, 1978. 14. Handa, J., Okamoto, K., and Sato, M.: Arachnoid cyst of the middle cranial fossa: Report of bilateral cysts in siblings. Surg. Neurol. 16: 127-130, 1981. IS. McCullough, D.C, Hargert, J.C, and Manz, H.J.: Large arachnoid cysts at the cranial base. Neurosurg. 6: 76-81, 1980. 16. Rosich-Pla, A, Smith, B.H., and Sil, R.: Congenital arachnoid cyst with unusual clinical, radiological and pathological findings. Ann. Neurol. 2(5): 443-446, 1977. 17. Murali, R., and Epstein, F.: Diagnosis and treatment of suprasellar arachnoid cyst. Report of three cases. ]. Neurosurg. 50: 515-518, 1979. 18. Lehman, R.A, and Fieger, H.G., Jr.: Arachnoid cyst producing recurrent neurological disturbances. Surg. Neurol. 10: 134-136, 1978. 19. Krohel, G.B., and Hepler, R.5.: Arachnoidal cyst invading the orbit. Arch. Ophthalmol. 97: 2342-2344, 1979. 20. Smith, J.L., Hoyt, W.F., and Susac, J.O.: Ocular fundus in acute leber optic neuropathy. Arch. Oph­thalmol. 90: 349-354, 1973. 21. Nikoskelainen, L, Sogg, R.L., Rosenthal, AR., et al.: The early phase in Leber hereditary optic atrophy. Arch. Ophthalmol. 95: 969-978, 1977. 22. Gittinger, J.W., Keltner, J.L., Miller, N.R., et al.: Progressive visual loss associated with peculiar disc swelling. SUTY. Ophthalmol. 24: 117-121, 1979. 23. Heckenlively, J.R., Martin, D.A, and Rosales, TO.: Telangiec (tasia and optic atrophy in cone-rod de­generations. Arch. Ophthalmol. 99: 1983-1991, 1981. 24. Wolter, J.R., and McKenney, M.J.: Collateral hyper­plasia and cyst formation of orbital leptomeninx. Am. ]. Ophthalmol. 57: 1037-1042, 1964. 25. Spencer, W.H.: Primary neoplasms of the optic nerve and its sheaths: Clinical features and current concepts of pathogenic mechanisms. Trans. Am. Ophthalmol. Soc. 70: 490-528, 1972. 26. Miller, N.R., and Green, R.W.: Arachnoid cysts in­volving a portion of the intra-orbital optic nerve. Arch. Ophthalmol. 93: 1117-1121, 1975. 27. Holt, H.: Cysts of the intracranial portion of the optic nerve. Am. ]. Ophthalmol. 61: 1166-1170, 1966. 28. deWecker, L.: On incision of the optic nerve in cases of neurorentinitis. Intemat. Ophthalmol. Congr. Rep. 4: 11, 1972. 29. Hayreh, 5.5.: Pathogenesis of oedema of the optic disc (papilloedema): A preliminary report. Br. ]. Ophthalmol. 48: 522-543, 1964. 30. Smith, J.L., Hoyt, W.F., and Newton, TH.: Optic nerve sheath decompression for relief of chronic monocular choked disc. Am. ]. Ophthalmol. 68: 191 Intr,lrr.1I1 i.J I 5ub.1I'<lchnoid Cysts t,33-b30 , 1969. 31, D,lVidson, 5.1.: A surgic.J1 approach to plerocephalic disc oedem.J. Tr,llls. Ophth,l/mo/. Soc u.K. 89: t'bQ-b90, IQbQ. 32. C.Jlbr,lith, I.E.K., .lllJ 5ulliv.Jn, I.H.: Decompression llf the pl'rioptic meninges for relief of pJpilledema. Am. /. Ophth,l/nlllJ. 76: b!\7-b92, 1973, 33, Burde, R.M., K,lrp, I.S, .1I1d Miller, R.: Reversal of visu,11 deficit with Optil' nerve decompression in longst,lnding pseudotumor cerebri. Am. /. Ophthdl­mol. 77: 770-772, 1974. Acknowledgments The authors thank Sandra Frazier-Byrne for perform­ing and interpreting the ultrasound studies. Write for reprints to: J. Lawton Smith, MD., Bascom Pidmer Eye Institute, P.O. Box 016880, Miami, Florida 33101. This study was supported in part by a Heed Oph­thalmic Fellowship (Dr. Conn). /' Journal of Clinical Neuro-ophthalmology