Arachnoidal Gregory
B.
Cyst Invading the Orbit
Krohel, MD, Robert S. Hepler, MD
glaucoma developed in a with a left-sided temporal 51-year-old lobe arachnoidal cyst. Ultrasonic examination disclosed a cystic orbital lesion adjacent to the optic nerve. Following intracranial decompensation of the arachnoidal cyst, the intraocular pressure dropped markedly. Ultrasonography showed a collapse of the presumed optic nerve sheath cyst. While the exact mechanism producing glaucoma in this patient remains unclear, there was an apparent relationship between the elevated intraocular pressure and the arachnoidal cyst. (Arch Ophthalmol 97:2342-2344, 1979) \s=b\ Ipsilateral
man
Arachnoidal cysts arising in the
"^
middle fossa are uncommonly diagnosed lesions that are either congenital (primary) or secondary to trauma
or
inflammation.1 These cysts
accompanied frequently by struc¬ tural skull deformities and agenesis of the temporal lobe.2 Arachnoidal cysts may remain asymptomatic, or they may produce headache, seizures, vi¬ sual field loss, cranial nerve palsies, and exophthalmos.'4 In addition, chronic papilledema and blepharopto¬ sis have been reported.3 Arachnoidal cysts of the optic nerve have been reported in association with gliomas,6 neurofibromas,7 the empty sella syndrome,8 and frontotemporal are
Accepted
for publication April 2, 1979. From the Department of Ophthalmology, Jules Stein Eye Institute, UCLA School of Medicine, Los Angeles. Dr Krohel is now with the Department of Ophthalmology, Albany (NY) Medical
College. Reprint requests
to Jules Stein Eye Institute, UCLA School of Medicine, Los Angeles, CA 90024
(Dr Hepler).
porencephalic cysts." They
have oc¬ curred also as isolated findings.910 A patient with an arachnoidal cyst of the temporal lobe developed exten¬ sion of the cyst through the optic canal into the orbit. Unilateral glaucoma with advanced cupping of the optic nerve head and visual field loss accom¬ panied extension of this arachnoidal
cyst.
REPORT OF A CASE
51-year-old
man was seen in neuroconsultation on July 5, 1978. He noted dimming of vision in the left eye for the previous four months with specific loss of peripheral vision nasally. He was also aware of increased prominence of his left eye during the same period. Continued observation by his local oph¬ thalmologist for three consecutive years prior to July 1978 included consistently normal intraocular pressures. The patient's general health was excellent, and findings of a neurologic workup in 1978 were normal. However, computerized axial to¬ mography revealed an area of low density in the left temporal lobe extending to the left optic foramen (Fig 1). No lesions were apparent in the limited views of the orbits that had been obtained. Examination confirmed a corrected vis¬ ual acuity of 20/20-1 in each eye. A mild degree of facial asymmetry was noted, with the left eye vertically displaced 1 to 2 mm higher in comparison with the right. Exophthalmometry readings were 18 mm on the right, 20 mm on the left. No orbital masses or orbital bruits were palpable. Both globes exhibited equal resistance to retrodisplacement. An afferent pupillary defect was present in the left eye. Ocular movements were full. Slit-lamp examina¬ tion of the anterior segment was normal bilaterally. Initial intraocular pressures were 25 mm Hg on the right and 35 mm Hg on the left by applanation tonometry.
A
ophthalmologic
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
Dilated ophthalmoscopic examination gave normal results in the right eye, with a cup/disc ratio of 0.3. The left fundus showed advanced glaucomatous optic atro¬ phy with a cup/disc ratio of 0.85 (Fig 2). Gonioscopy showed both anterior chamber angles to be widely open with no discerni¬ ble abnormalities. Goldmann perimetry was normal in the right eye and disclosed a large inferior arcuate scotoma in the left eye. Topical 2% epinephrine hydrochloride opthalmic solution applied twice daily to the left eye reduced the intraocular pres¬ sure to 23 mm Hg, and the pressure of the untreated right eye was also 23 mm Hg. Tonography provided a coefficient of outflow or C value of 0.19 in both the right and left eyes. On B-scan ultrasonography a cystic mass was shown at the 6-o'clock meridian in the orbital apex of the left eye. This lesion was adjacent and inferior to the left optic nerve (Fig 3). The cystic nature of the mass was confirmed on A-scan, where compression reduced the size of the mass from 6.2 mm to 5.0 mm (Fig 4). Basal tomography of the
Fig 1.—Intra-arachnoidal cyst seen with computerized tomography as low-density area occupying left middle fossa (arrows) with elongation of anterior aspect of left middle fossa.
Fig 2—Left optic nerve (left) showing advanced glaucomatous cupping right (right).
Fig 4.—Cystic
in
comparison to
3.—B-scan ultrasonography revealing lesion (wide arrows) adjacent and inferior to left optic nerve (narrow arrows).
Fig
nature of lesion confirmed by A-scan ultrasonography. Compression mass from (left) 6.2 mm (arrows) to (right) 5.0 mm (arrows).
reduces size of
skull demonstrated asymmetry of the ante¬ rior margins of the middle fossa with the left middle fossa extending more anterior¬ ly than the right. A carotid arteriogram disclosed displacement of the middle cere¬ bral artery and its branches superiorly and medially, consistent with an avascular left temporal mass lesion. Roentgenographically, the optic canals were symmetric and
enlarged. patient underwent a left frontal craniotomy. An arachnoidal cyst was found to occupy the anterior portion of the left temporal fossa. The cyst extended to the optic canal, and under the surgical micro¬
were
not
The
scope, it
optic
was seen
to enter the canal. The
displaced medially by the cyst, which was decompressed surgically and excised where possible within the cra¬ nerve was
nial vault. No attempt was made to unroof the optic canal or explore the orbit. Patho¬ logic examination showed sections of fibrous tissue with meningothelial-like cells consistent with an arachnoidal cyst
wall. The postoperative course was compli¬ cated transiently by an epidural hematoma at one week after surgery. After surgical evacuation of the hematoma, the patient did well, and three weeks after surgery, he was reexamined while receiving no glauco¬ ma medication. Intraocular pressures were 23 mm Hg on the right and 24 mm Hg on the left. Repeat B-scan ultrasonography showed a minimal defect below and nasal to the left optic nerve (Fig 5). A-scan ultrasonography results were entirely nor¬ mal. The patient received 1% epinephrine applied to both eyes twice daily, and six weeks later, the intraocular pressures were 16 mm Hg on the right and 18 mm Hg on the left by applanation tonometry. Repeat exophthalmometry readings were 18 mm on the right and 19 mm on the left. COMMENT
The association of an intracranial arachnoidal cyst with an optic nerve
Fig 5.—Repeat B-scan ultrasonography after intracranial decompression of arach¬ noid cyst, revealing almost complete reso¬ lution of the orbital lesion (arrows).
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
cyst is unusual. A previous report
proposed that an intrasellar arachnoi¬ dal cyst was responsible for the ap¬ pearance of an "empty sella" syn¬ drome, which
was
associated with
surgically observed optic The presence of
an
a
cyst. arachnoidal cyst, nerve
however, was not proved pathological¬ ly/ Another report described an optic nerve
cyst that
was
associated with
a
porencephalic cyst in the frontotemporal region." This cyst was thought to represent, possibly, a response to repeated bouts of increased intracra¬ nial pressure. It was postulated that
the cyst formation resulted from transmitted pressure along the vagi¬ nal sheath of the optic nerve. This latter mechanism may indeed have played a role in the formation of the orbital cyst in the present patient. Pathologic confirmation of an optic nerve cyst is not available in the pres¬ ent patient. The compressibility of the lesion on ultrasonic examination, how¬ ever, is highly suggestive of a cystic lesion. In addition, the intracranial cyst wall was adherent to the optic nerve at its entrance into the optic canal, and it extended into the canal displacing the nerve medially. These findings, in addition to the shrinkage of the orbital lesion after intracranial decompression of the temporal lobe cyst, strongly suggest an anatomic connection between the two.
Another noteworthy aspect of this involves the unilateral advanced glaucoma, interpretation of which is difficult in view of the borderline C values in both eyes and the initial asymmetric elevation of pressure in both eyes. Also, there was a pro¬ nounced drop in intraocular pressure in both eyes after treatment with 1% epinephrine twice a day. After surgi¬ cal decompression of the intracranial cyst, however, intraocular pressure decreased dramatically in the ipsilat¬ eral eye. Furthermore, the left eye developed both visual field and visible optic nerve abnormalities consistent with glaucoma, and these glaucoma indications were not present at all in the right eye. Accordingly, it is diffi¬ cult not to suspect a causal relation¬ ship between the arachnoidal cyst and the clinical signs of glaucoma in the left eye. Glaucoma has been reported in association with orbital obstructive lesions, presumably on the basis of increased episcleral venous pres¬ sure." ·'- This mechanism seems un¬ likely in our patient, however, as no episcleral vessels or reflux of blood in Schlemm's canal were prominent on gonioscopic examination. Episcleral venous pressures were not measured. Orbital mass lesions can lead to secondary angle-closure glaucoma, but normal anterior chamber findings on slit-lamp examination and gonioscopy case
rule out that
patient.
possibility
in
this
It is believed that arachnoidal cysts communicate intermittently with the subarachnoid space.' Moreover, pro¬ gressive distention of such cysts may result from CSF pulsations of venous origin." It is proposed that intermit¬ tent venous pulsations caused pro¬ gressive distention of a congenital arachnoidal cyst, the enlargement then being transmitted into the vagi¬ nal sheath of the optic nerve to form an optic nerve cyst. This communica¬ tion between the orbital cyst and the intracranial cyst may have been inter¬ rupted intermittently, with a resul¬ tant disparity between intraorbital optic sheath pressure and intracranial optic nerve pressure. A relatively high-to-low pressure gradient from orbital optic nerve to intracranial optic nerve may have contributed to compromise of blood perfusion in the optic nerve already embarrassed by a preexisting ocular hypertension. Optic disc cupping has been produced in cats by lowering intracranial pressure by means of a cannula inserted into the cisterna magna." The actual mecha¬ nism that produced glaucoma in our patient remains uncertain. Viesturs T. Verona
patient. tance.
Petersons, MD, referred the Pettyjohn gave editorial assis¬
References 1. Grollmus JM, Wilson CB, Newton TH: Paramesencephalic arachnoid cysts. Neurology
26:128-134, 1976.
2. Lindenberg R, Walsh FB, Sacks JG: Neuropathology of Vision: An Atlas. Philadelphia, Lea & Febiger, 1973, pp 190-193.
3. Seur NH, Kooman A: Arachnoid cyst of the middle fossa with paradoxical changes of the
bony
structures. 1976. 4. Walsh FG,
Neuroradiology 12:177-183,
Hoyt WF: Clinical ophthalmology. Baltimore, Williams &
NeuroWilkins
Co, 1969, vol 3, pp 2193-2195. 5. Dyck P, Gruskin P: Supratentorial arachnoid cysts in adults. Arch Neurol 34:276-279, 1977.
6. Wolter JR, McKenney MJ: Collateral hyperand cyst formation of orbital leptomenix. Am J Ophthalmol 57:1037-1042, 1964. 7. Spencer WH: 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. 8. Smith JL, Hoyt WF, Newton TH: Optic nerve sheath decompression for relief of chronic monocular choked disc. Am J Ophthalmol 68:633\x=req-\ 639, 1969. 9. Miller NR, Green RW: Arachnoid cysts involving a portion of the intraorbital optic nerve. Arch Ophthalmol 93:1117-1121, 1975. 10. Holt H: Cysts of the intracranial portion of the optic nerve. Am J Ophthalmol 61:1166-1170,
plasia
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
1966. 11. Kolker
AE, Hetherington J (eds): Becker\x=req-\ Shaffer's Diagnosis and Therapy of the Glaucomas. St Louis, CV Mosby Co, 1976, pp 267-269. 12. Morin JD: Secondary glaucoma, in Duane T (ed): Clinical Ophthalmology. Hagerstown, Md, Harper & Row Publishers, vol 3, 1976, p 8. 13. Williams B. Guthfelch AN: Why do central arachnoid pouches expand? J Neurol Neurosurg Psychiatry 37:1085-1092, 1974. 14. Yablonski ME, Krupin T, Becker B: Deceased intracranial pressure and optic disc cupping in the cat, abstracted Invest Ophthalmol Vis Sci 17(suppl):186, 1978.
B.
Cyst Invading the Orbit
Krohel, MD, Robert S. Hepler, MD
glaucoma developed in a with a left-sided temporal 51-year-old lobe arachnoidal cyst. Ultrasonic examination disclosed a cystic orbital lesion adjacent to the optic nerve. Following intracranial decompensation of the arachnoidal cyst, the intraocular pressure dropped markedly. Ultrasonography showed a collapse of the presumed optic nerve sheath cyst. While the exact mechanism producing glaucoma in this patient remains unclear, there was an apparent relationship between the elevated intraocular pressure and the arachnoidal cyst. (Arch Ophthalmol 97:2342-2344, 1979) \s=b\ Ipsilateral
man
Arachnoidal cysts arising in the
"^
middle fossa are uncommonly diagnosed lesions that are either congenital (primary) or secondary to trauma
or
inflammation.1 These cysts
accompanied frequently by struc¬ tural skull deformities and agenesis of the temporal lobe.2 Arachnoidal cysts may remain asymptomatic, or they may produce headache, seizures, vi¬ sual field loss, cranial nerve palsies, and exophthalmos.'4 In addition, chronic papilledema and blepharopto¬ sis have been reported.3 Arachnoidal cysts of the optic nerve have been reported in association with gliomas,6 neurofibromas,7 the empty sella syndrome,8 and frontotemporal are
Accepted
for publication April 2, 1979. From the Department of Ophthalmology, Jules Stein Eye Institute, UCLA School of Medicine, Los Angeles. Dr Krohel is now with the Department of Ophthalmology, Albany (NY) Medical
College. Reprint requests
to Jules Stein Eye Institute, UCLA School of Medicine, Los Angeles, CA 90024
(Dr Hepler).
porencephalic cysts." They
have oc¬ curred also as isolated findings.910 A patient with an arachnoidal cyst of the temporal lobe developed exten¬ sion of the cyst through the optic canal into the orbit. Unilateral glaucoma with advanced cupping of the optic nerve head and visual field loss accom¬ panied extension of this arachnoidal
cyst.
REPORT OF A CASE
51-year-old
man was seen in neuroconsultation on July 5, 1978. He noted dimming of vision in the left eye for the previous four months with specific loss of peripheral vision nasally. He was also aware of increased prominence of his left eye during the same period. Continued observation by his local oph¬ thalmologist for three consecutive years prior to July 1978 included consistently normal intraocular pressures. The patient's general health was excellent, and findings of a neurologic workup in 1978 were normal. However, computerized axial to¬ mography revealed an area of low density in the left temporal lobe extending to the left optic foramen (Fig 1). No lesions were apparent in the limited views of the orbits that had been obtained. Examination confirmed a corrected vis¬ ual acuity of 20/20-1 in each eye. A mild degree of facial asymmetry was noted, with the left eye vertically displaced 1 to 2 mm higher in comparison with the right. Exophthalmometry readings were 18 mm on the right, 20 mm on the left. No orbital masses or orbital bruits were palpable. Both globes exhibited equal resistance to retrodisplacement. An afferent pupillary defect was present in the left eye. Ocular movements were full. Slit-lamp examina¬ tion of the anterior segment was normal bilaterally. Initial intraocular pressures were 25 mm Hg on the right and 35 mm Hg on the left by applanation tonometry.
A
ophthalmologic
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
Dilated ophthalmoscopic examination gave normal results in the right eye, with a cup/disc ratio of 0.3. The left fundus showed advanced glaucomatous optic atro¬ phy with a cup/disc ratio of 0.85 (Fig 2). Gonioscopy showed both anterior chamber angles to be widely open with no discerni¬ ble abnormalities. Goldmann perimetry was normal in the right eye and disclosed a large inferior arcuate scotoma in the left eye. Topical 2% epinephrine hydrochloride opthalmic solution applied twice daily to the left eye reduced the intraocular pres¬ sure to 23 mm Hg, and the pressure of the untreated right eye was also 23 mm Hg. Tonography provided a coefficient of outflow or C value of 0.19 in both the right and left eyes. On B-scan ultrasonography a cystic mass was shown at the 6-o'clock meridian in the orbital apex of the left eye. This lesion was adjacent and inferior to the left optic nerve (Fig 3). The cystic nature of the mass was confirmed on A-scan, where compression reduced the size of the mass from 6.2 mm to 5.0 mm (Fig 4). Basal tomography of the
Fig 1.—Intra-arachnoidal cyst seen with computerized tomography as low-density area occupying left middle fossa (arrows) with elongation of anterior aspect of left middle fossa.
Fig 2—Left optic nerve (left) showing advanced glaucomatous cupping right (right).
Fig 4.—Cystic
in
comparison to
3.—B-scan ultrasonography revealing lesion (wide arrows) adjacent and inferior to left optic nerve (narrow arrows).
Fig
nature of lesion confirmed by A-scan ultrasonography. Compression mass from (left) 6.2 mm (arrows) to (right) 5.0 mm (arrows).
reduces size of
skull demonstrated asymmetry of the ante¬ rior margins of the middle fossa with the left middle fossa extending more anterior¬ ly than the right. A carotid arteriogram disclosed displacement of the middle cere¬ bral artery and its branches superiorly and medially, consistent with an avascular left temporal mass lesion. Roentgenographically, the optic canals were symmetric and
enlarged. patient underwent a left frontal craniotomy. An arachnoidal cyst was found to occupy the anterior portion of the left temporal fossa. The cyst extended to the optic canal, and under the surgical micro¬
were
not
The
scope, it
optic
was seen
to enter the canal. The
displaced medially by the cyst, which was decompressed surgically and excised where possible within the cra¬ nerve was
nial vault. No attempt was made to unroof the optic canal or explore the orbit. Patho¬ logic examination showed sections of fibrous tissue with meningothelial-like cells consistent with an arachnoidal cyst
wall. The postoperative course was compli¬ cated transiently by an epidural hematoma at one week after surgery. After surgical evacuation of the hematoma, the patient did well, and three weeks after surgery, he was reexamined while receiving no glauco¬ ma medication. Intraocular pressures were 23 mm Hg on the right and 24 mm Hg on the left. Repeat B-scan ultrasonography showed a minimal defect below and nasal to the left optic nerve (Fig 5). A-scan ultrasonography results were entirely nor¬ mal. The patient received 1% epinephrine applied to both eyes twice daily, and six weeks later, the intraocular pressures were 16 mm Hg on the right and 18 mm Hg on the left by applanation tonometry. Repeat exophthalmometry readings were 18 mm on the right and 19 mm on the left. COMMENT
The association of an intracranial arachnoidal cyst with an optic nerve
Fig 5.—Repeat B-scan ultrasonography after intracranial decompression of arach¬ noid cyst, revealing almost complete reso¬ lution of the orbital lesion (arrows).
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
cyst is unusual. A previous report
proposed that an intrasellar arachnoi¬ dal cyst was responsible for the ap¬ pearance of an "empty sella" syn¬ drome, which
was
associated with
surgically observed optic The presence of
an
a
cyst. arachnoidal cyst, nerve
however, was not proved pathological¬ ly/ Another report described an optic nerve
cyst that
was
associated with
a
porencephalic cyst in the frontotemporal region." This cyst was thought to represent, possibly, a response to repeated bouts of increased intracra¬ nial pressure. It was postulated that
the cyst formation resulted from transmitted pressure along the vagi¬ nal sheath of the optic nerve. This latter mechanism may indeed have played a role in the formation of the orbital cyst in the present patient. Pathologic confirmation of an optic nerve cyst is not available in the pres¬ ent patient. The compressibility of the lesion on ultrasonic examination, how¬ ever, is highly suggestive of a cystic lesion. In addition, the intracranial cyst wall was adherent to the optic nerve at its entrance into the optic canal, and it extended into the canal displacing the nerve medially. These findings, in addition to the shrinkage of the orbital lesion after intracranial decompression of the temporal lobe cyst, strongly suggest an anatomic connection between the two.
Another noteworthy aspect of this involves the unilateral advanced glaucoma, interpretation of which is difficult in view of the borderline C values in both eyes and the initial asymmetric elevation of pressure in both eyes. Also, there was a pro¬ nounced drop in intraocular pressure in both eyes after treatment with 1% epinephrine twice a day. After surgi¬ cal decompression of the intracranial cyst, however, intraocular pressure decreased dramatically in the ipsilat¬ eral eye. Furthermore, the left eye developed both visual field and visible optic nerve abnormalities consistent with glaucoma, and these glaucoma indications were not present at all in the right eye. Accordingly, it is diffi¬ cult not to suspect a causal relation¬ ship between the arachnoidal cyst and the clinical signs of glaucoma in the left eye. Glaucoma has been reported in association with orbital obstructive lesions, presumably on the basis of increased episcleral venous pres¬ sure." ·'- This mechanism seems un¬ likely in our patient, however, as no episcleral vessels or reflux of blood in Schlemm's canal were prominent on gonioscopic examination. Episcleral venous pressures were not measured. Orbital mass lesions can lead to secondary angle-closure glaucoma, but normal anterior chamber findings on slit-lamp examination and gonioscopy case
rule out that
patient.
possibility
in
this
It is believed that arachnoidal cysts communicate intermittently with the subarachnoid space.' Moreover, pro¬ gressive distention of such cysts may result from CSF pulsations of venous origin." It is proposed that intermit¬ tent venous pulsations caused pro¬ gressive distention of a congenital arachnoidal cyst, the enlargement then being transmitted into the vagi¬ nal sheath of the optic nerve to form an optic nerve cyst. This communica¬ tion between the orbital cyst and the intracranial cyst may have been inter¬ rupted intermittently, with a resul¬ tant disparity between intraorbital optic sheath pressure and intracranial optic nerve pressure. A relatively high-to-low pressure gradient from orbital optic nerve to intracranial optic nerve may have contributed to compromise of blood perfusion in the optic nerve already embarrassed by a preexisting ocular hypertension. Optic disc cupping has been produced in cats by lowering intracranial pressure by means of a cannula inserted into the cisterna magna." The actual mecha¬ nism that produced glaucoma in our patient remains uncertain. Viesturs T. Verona
patient. tance.
Petersons, MD, referred the Pettyjohn gave editorial assis¬
References 1. Grollmus JM, Wilson CB, Newton TH: Paramesencephalic arachnoid cysts. Neurology
26:128-134, 1976.
2. Lindenberg R, Walsh FB, Sacks JG: Neuropathology of Vision: An Atlas. Philadelphia, Lea & Febiger, 1973, pp 190-193.
3. Seur NH, Kooman A: Arachnoid cyst of the middle fossa with paradoxical changes of the
bony
structures. 1976. 4. Walsh FG,
Neuroradiology 12:177-183,
Hoyt WF: Clinical ophthalmology. Baltimore, Williams &
NeuroWilkins
Co, 1969, vol 3, pp 2193-2195. 5. Dyck P, Gruskin P: Supratentorial arachnoid cysts in adults. Arch Neurol 34:276-279, 1977.
6. Wolter JR, McKenney MJ: Collateral hyperand cyst formation of orbital leptomenix. Am J Ophthalmol 57:1037-1042, 1964. 7. Spencer WH: 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. 8. Smith JL, Hoyt WF, Newton TH: Optic nerve sheath decompression for relief of chronic monocular choked disc. Am J Ophthalmol 68:633\x=req-\ 639, 1969. 9. Miller NR, Green RW: Arachnoid cysts involving a portion of the intraorbital optic nerve. Arch Ophthalmol 93:1117-1121, 1975. 10. Holt H: Cysts of the intracranial portion of the optic nerve. Am J Ophthalmol 61:1166-1170,
plasia
Downloaded From: http://archopht.jamanetwork.com/ by a Michigan State University User on 06/18/2015
1966. 11. Kolker
AE, Hetherington J (eds): Becker\x=req-\ Shaffer's Diagnosis and Therapy of the Glaucomas. St Louis, CV Mosby Co, 1976, pp 267-269. 12. Morin JD: Secondary glaucoma, in Duane T (ed): Clinical Ophthalmology. Hagerstown, Md, Harper & Row Publishers, vol 3, 1976, p 8. 13. Williams B. Guthfelch AN: Why do central arachnoid pouches expand? J Neurol Neurosurg Psychiatry 37:1085-1092, 1974. 14. Yablonski ME, Krupin T, Becker B: Deceased intracranial pressure and optic disc cupping in the cat, abstracted Invest Ophthalmol Vis Sci 17(suppl):186, 1978.
