Progressive visual loss with normal examination. A conundrum

SURVEY OF OPHTHALMOLOGY

VOLUME 30

??

NUMBER 4 -JANUARY-FEBRUARY

1966

CLINICAL CHALLENGES RONALD M. BURDE AND PAUL HENKIND, EDITORS

Progressive Visual Loss With Normal Examination. A Conundrum THOMAS

L. SLAMOVITS,

M.D.,l

AND

RONALD

M. BURDE,

M.D.2

Comments by Neil R. Miller, M.D., John W. Gittinger, Jr., M.D., and John L. Keltner, M.D.

University ofpittsburgh Eye and Ear Hospital, Pittsburgh, Pennsylvania, and ‘De artment of Ophthalmology, 4) the Departments of Ophthalmology and Neurology and Neurological Surgery, Washington University School of Medicine, St. Louis, Missouri (In keeping with the article.)

A 68-year-old plaints

thepur$ose ofa clinical pathological

white woman

until mid-February,

had no visual

1985,

when

bilateral visual blurring and perceived “dull.” Past medical history was positive derline”

diabetes

Optometric acuities

and

examination

were reported

“borderline” was as 20120

conference, the abstract

Eye and Ear

com-

perception”

colors as for “borand

in both

Computerized

(10 mm cuts for “bilateral occipital and visual evoked response in normal.

tomographic

amination

pupils

motility,

1) were normal (Fig.

did not re-

light stimulato convergence. and fundus ex-

in both eyes. A CT

2).

What is your dtyerential diagnosis?

scan

Comments

lobe infarction”) both eyes were

Comments by Neil R. Miller, M.D., The Wilmer Ofihthalmological Institute, Johns Hopkins Hospital, Baltimore, Maryland This 68-year-old woman, who was previously relatively healthy, suffered bilateral progressive visual loss and became virtually blind over a 2-3 week period. In such a patient, the initial issue is the

started on oral prednisone. A temporal artery biopsy was negative. One week later vision was “light perception” in both eyes. Seven weeks after her initial complaints began, was seen at the University

The

or consensual

exam, extraocular (Fig.

examina-

a visual acuity of “no light

eyes.

to direct

scan was repeated

pre-

Vision deteriorated further, and the patient saw another ophthalmologist the following week. Vision was “hand motions” in both eyes. An erythrocyte sedimentation rate was 57 mm/hr, and she was

the patient

Ophthalmologic

tion, but there was good response External

visual

cipitously, and she saw an ophthalmologist. Vision was “linger counting” in both eyes. She was referred to a neurologist.

in both

spond either

eyes.

Two to three weeks later vision deteriorated

Hospital.

tion at that time revealed

she noted

hypertension.

normal,

and key words appear at the end of

location of the lesion. I would expect that retinal lesions producing such a profound visual loss would be quite obvious during an ophthalmoscopic exami-

of Pittsburgh 251

252

Surv Ophthalmol

Fig. I. Left: Normal demonstrating

fundus questionable

30(4) January-February

1986

photograph of the patient’s optic disc pallor.

The patient might also be expected to have poor pupillary responses to direct light stimulation, A process involving both optic nerves or the optic chiasm might produce any type of visual field defect and reduced pupillary light responses. Any process posterior to the optic chiasm but anterior to the lateral geniculate body might also be expected to be associated with poor pupillary light responses and, in addition, with bilateral homonymous hemianopic visual field defects. Finally, any process involving the retrogeniculate visual sensory pathway must clearly be bilateral. Pupillary responses would be relatively normal despite profound visual loss, but the visual fields might be expected to have a hemianopic flavor. Unfortunately, we are given no information regarding the pupillary responses or the visual fields of the patient when she was first seen by an ophthalmologist. It is therefore impossible to localize the lesion at this stage of her disorder. The assumption made by the examining neurologist that the patient’s visual loss was caused by a bilateral occipital lobe infarction might be reasonable if the patient had normal pupillary responses. A CT scan with 10 mm cuts might identify such a lesion, but I would have favored much thinner cuts, not only for evaluation of the occipital lobes but also for evaluation of the rest of the visual pathway. It should also be remembered that in many acute infarctions an immediate CT scan may not show any abnormality and that obvious changes might not be apparent for 7-10 days. The availability of magnetic resonance imaging should obviate this problem. The fact that a visual evoked response in both eyes was “normal” does not, of itself, mean much to me. We are not told how it was performed or what nation.

right

SLAMOVITS,

eye. Right:

Fundus

photograph

of the patient’s

BURDE

left eye

criteria were used. In addition, there have been some patients with cortical blindness who have been said to have “normal” visual evoked responses, perhaps because the pathways that mediate the visual evoked response are anterior to the lesion, in the prestriate cortical region.‘+j On the other hand, I certainly would have expected a process involving the optic nerves or chiasm to produce a markedly abnormal visual evoked response, even one performed only with a flash stimulus, as I presume this one was. When vision deteriorated further, the patient saw another ophthalmologist who found vision of “hand motions” in each eye and was concerned about the possibility of temporal arteritis. An erythrocyte sedimentation rate was elevated, the patient was begun on prednisone, and a temporal artery biopsy was performed. It was negative. Although we are not told if this patient had any clinical symptoms of temporal or giant cell arteritis (for example, scalp tenderness, jaw claudication, ear pain, migratory arthralgias, night sweats, etc.), I believe the ophthalmologist was absolutely correct in considering this diagnosis. The occurrence of precipitous visual loss, monocular or binocular, in an elderly patient should always raise the spectre of temporal arteritis. Even when bilateral visual loss has occurred, diagnosis and treatment of the disorder may prevent other vascular catastrophes involving the brain, heart, or kidneys from occurring. It should also be remembered that any patient suspected of having temporal arteritis should be placed on corticosteroids immediately and then have a temporal artery biopsy, as was apparently done in this case. An involved temporal artery will remain abnormal

VISUAL

LOSS WITH NORMAL

253

EXAMINATION

Kg. 2. Left: CT scan demonstrating thickening ofthe optic nerves and chiasm. Right: CT scan demonstrating of the optic chiasm and left optic tract. teristic

syndrome.6J0*,‘5J0

The

from a histologic standpoint for at least eight days (and probably longer) following initiation of steroid

monocular

blurring

therapy. A mere seven weeks following

simulating

optic neuritis

athy. The fundus

her initial eye com-

appear

normal,

plaints, the patient was completely blind with no pupillary reactions to light stimulation. The fundi,

evidence

however,

optic

tion

remained

of the

normal.

process

At this point,

becomes

clear.

the loca-

On

clinical

or ischemic

of the involved

are

vascular

pain,

optic neurop-

eye may initially

but most patients

including

swelling. There

symptoms

of vision and retrobulbar

of occlusive

disc,

initial

thickening

rapidly

develop

disease

involving

the

stasis,

edema,

and

venous

may be extensive

hemorrhage

in the

grounds alone, it must involve the intracranial portions of the optic nerves or the optic chiasm. A high

posterior pole, and the fundus picture may thus be one of central retinal vein occlusion or venous stasis

resolution

retinopathy. Neovascular glaucoma may develop. This does not remain, however, a monocular dis-

CT

the location sion.

scan performed

of what

appears

In my opinion,

produces

there

this syndrome

nant glioma

at this time verifies to be an intrinsic

is only one lesion

in this age group:

of the anterior

visual

lethat

a malig-

pathways.

ease. Within involved,

cits develop.

and a generally

year.

cytomas system,

do occasionally producing

prognosis, involve

a catastrophic

malignant

astro-

the anterior

visual

clinical

picture

of

is soon completely

blind.

In the latter stages of the disease, hypothalamic dysfunction, hemiparesis, and other neurologic defi-

While most gliomas that involve the anterior visual pathways have a benign histologic appearance benign

5-6 weeks, both eyes will have become

and the patient

Death

Malignant nially

usually

optic gliomas

produce

a similar

occurs

in less than one

that originate syndrome

intracra-

of progressive

progressive visual loss, neurologic deficits, and death. Unlike low-grade gliomas of the anterior visual system that occur in children, malignant glio-

visual loss, neurologic symptomatology, However, the visual loss in these patients

mas

with normal appearing or pale optic discs.5~7,20J Th e pathologic features of the malignant optic glioma are characteristic. The vascular and partial-

virtually

some reports

always suggest

marily in men, Spoor

occur

in adults.

that these

tumors

Although occur

pri-

and associateszO reviewed

the

previously reported cases and noted that of 26 patients, 15 were men and 11 were women. The ages of these patients ranged from 22-79 years with an average

of 5 1.9 years.

The specific pattern patients with malignant

of visual loss occurring gliomas of the anterior

in vi-

sual pathways appears to depend on the site of origin of the tumor. Tumors originating in the distal portion of one of the optic nerves produce a charac-

and simultaneous

(or nearly

so) and is associated

ly necrotic tumor occupies most optic chiasm, and optic tracts. tumor has invariably spread to and adjacent parts of the brain. usually infiltrated surrounding

the meninges

soft tissue.

*See the bibliography earlier references.

The

of Reference

and death. is bilateral

of the optic nerves, Intracranially, the the hypothalamus In the orbit, it has of the nerve and the

histopathology

of this

# 10 for a more complete

list of

Surv Ophthalmol

254

30(4) January-February

tumor, as might be expected, from that of the typical curs primarily

is completely

cellular

and scattered

numerous

of vascular

tion, necrosis,

features

a biopsy

of malignant

ways is probably

tem, but increasing

hy-

member

are

giomas were rarely diagnosed ploration.

prolifera-

that only a decade

Malignant

to confirm

glioma

awareness

the presumed

of the visual

path-

after which radiother-

pathway

benign

glioma,

tation of malignant

of

no

retrobulbar

ra-

tient is characteristically

the

deteriorates

treatment

diotherapy

for this condition.

nor chemotherapy

inexorable

progression

appears

from blindness

to be hoped that some method tunate patients

Neither to halt to death.

of helping

It is

the unfor-

with this tumor will be developed

in

time.

This

6%year-old

sive bilateral

woman

visual

scopic examination. considered,

but

eventually

had subacute

loss with a normal Initially,

pupillary

lost. The

cortical

to light

is therefore

the optic tracts,

where the axons subserving to light exit the visual

Another

consideration

cell arteritis. mentation ative

The

rate supports

temporal

exclude

artery

it9 The

pain on chewing,

this diagnosis,

presence

giant cell arteritis,

does

of other

weight

was giant sedi-

and the neg-

not completely clinical

loss, malaise,

scalp tenderness,

girdles is not mentioned.

the pu-

of the erythrocyte

biopsy

signs

Hayreh8 reports

Both anterior

of

headache,

pains in the limb

If this were giant cell arte-

ritis, the patient would have either a bilateral rior ischemic optic neuropathy or an ischemic ma1 syndrome.

to

pathways.

in this patient

elevation

were

anterior

pillary

reaction

was

of these ischemic

in one eye as a presentation

entities

postechias-

are

rare.

optic neuropathy

of temporal

arteritis,

followed two months later by loss of visual field, with relative preservation of acuity attributed to posterior ischemic optic neuropathy. Lee and associates14 include giant cell arteritis in the differential diagnosis of the ischemic chiasmal syndrome, but the case

they

present

as an example

is not

vincing. This patient probably has a malignant nerve glioma of adulthood, perhaps better

conoptic called

to the visual

management

Unlike

optic

re-

presen-

an optic or

neuritis,

middle-aged,

the pa-

and vision

over a period of weeks, sometimes

cular occlusions.

picture When

resembling

with

retinal

first described,

vas-

a male pre-

ponderance was noted, but this was probably an artifact of discovery. In all reported cases, death within

a few months

of presentation,

even

with treatment. Most

cases in the literature

are from the pre- or

early CT

scan era, and even appropriate

diological

studies

resolution

CT

enlargement

ophthalmoblindness

reactions

process

progres-

optic glioma

neuritis.

an ophthalmoscopic

ensued

Comments by John W. Gittinger, Jr., M.D., Division of Ophthalmology, University of Massachusetts, Worcester, Massachusetts

cousin

mimics

How-

I

satisfactory

whose

ex-

anterior

The initial

be attempted. aware

is a distant

a tumor

time,

am

and

at surgical

mains a topic of controversy.17J5

might

present

except

or “childhood”

apy or chemotherapy the

of its existence

ago optic nerve menin-

optic glioma

more familiar

ever,

at

BURDE

the availability of improved imaging techniques seem certain to improve diagnostic accuracy. Re-

There

mitoses. endothelial

reasonable,

SLAMOVITS,

nuclear

and hemorrhage.

In this patient, diagnosis

that oc-

Characteristic

pleomorphism,

perchromaticity, areas

different

optic nerve glioma

in childhood.

include extreme

1986

glioma,

are usually

scan obtained of the chiasm

as would

neurora-

negative.21

The

on this patient similar

highshows

to a childhood

be predicted.

The finding that is most difficult to explain is the normal visual evoked response. I would expect a patient with “linger

counting”

have an extinguished

pattern

potential.

vision in both eyes to or flash visual evoked

In view of the probable

even more difficult

diagnosis,

to understand,

visual evoked response abnormalities adults with benign optic glioma.13 Are there other

diagnostic

this is

since prominent are seen

possibilities?

Cases

in of

sarcoidosis simulate glioma clinically,‘8J3 and lymphoma is always a possibility. Miller even describes two cases where biopsies rior visual

system

glioma.17 One the other, While

turned

a reticulum sharing

of mass lesions of the ante-

were initially

as

disease;

cell sarcoma.

the assessment

leagues 25 that biopsies

misinterpreted

out to be Hodgkin’s

are rarely

of Wright

and col-

useful in the man-

agement of benign childhood glioma, I would obtain a surgical specimen in this situation. If this is a malignant optic glioma, the prognosis is extremely poor.

Comments by John L. Keltner, M.D., Departments of Ophthalmology, Neurology, and Neurosurgery, UniversiQ of California at Davis, Davis, California

malignant glioma of the optic nerve pathways or Malignant optic malignant optic glioma. 7~10,15,16,20 glioma has been difficult to recognize without his-

A 68-year-old woman who was previously in good health until mid-February, 1985, suddenly noted bilateral blurring of vision and perceived colors as

tology,

“dull.”

either from transcranial

biopsy

or postmor-

Visual

acuities

were

recorded

as 20120

in

VISUAL

LOSS WITH NORMAL

255

EXAMINATION

both eyes. However, 2-3 weeks later she had precipitous loss of vision to “finger counting” and was referred to a neurologist who found “linger counting” vision. Also, a computerized scan with 10 mm

patient

cuts and a visual evoked potential

patient on prednisone. A temporal artery biopsy was negative. One week later the vision was “light

were reported

as

normal. Approximately five weeks later she saw an ophthalmologist and had “hand motions” vision with

an

erythrocyte

sedimentation

mm/hr. She had a negative was started had “light

temporal

on oral prednisone, perception”

in both

after her initial complaints time we were

told

of evaluation.

and was referred

rate

perception.” pupils,

of 57 mm/hr,

Again,

While certainly

a 68-year-old

weeks

erythrocyte

tion that this patient had other cell arteritis.12 Giant cell arteritis

was the first

her

pupils.

They

were

to have giant cell arteritis

The patient found

was initial-

seen,*

there

giant cell arteritis.

Thus,

response to light, would be assumed sion. Actually,

posterior

in this

patient,

and

I doubt

worthy

of entertaining

in this

tests to count-

as well as showed

no

to the chiasm

case. seven weeks into her illness,

at which time

her vision was “no light perception”

and her pupils

did not respond to light but were responsive to convergence. It took four examinations until she had a pupil exam that was recorded, patient

had

no remaining

would be of no help.

The

and by that time the

vision, pupils

light but reacted

istic visual field defect.

such as

ably in the region

of the chiasm.

might

tion was reported

as normal

progressive have been certainly

detected

degeneration,

by looking

an electroretinogram

the correct reported

photoreceptor

diagnosis.

as normal,

pathology,

A visual evoked potential was performed

rience of the testing laboratory. eral reported cases of patients visual

nor the expe-

While there are sevwith cortical blind-

evoked

potentials,

that this was the case in this patient.3,‘J2 visual evoked response when

the

pupillary

was

was improperly examination

and

I doubt Thus,

the

relied upon the

visual

fields were the important tests to be performed at the time. In addition, 10 mm cuts for an occipital lobe lesion

are too thick,

along with coronal

and

thinner

cuts of the occipital

axial

cuts

lobe would

have been much better for demonstrating an occipital lobe lesion. In addition, recent articles attest to the superior ability of magnetic resonance imaging to find certain lesions in the cerebral hemispheres not demonstrated on CT scan. This is particularly true in demyelinating disease and is seen in congenital abnormalities.1*24 In addition, there is no indication of CT scan examination of the chiasm in the

to convergence,

patient had an anterior

but

but we are not told what type of

visual evoked potential

ness and normal

at the retina,

would have provided

the patient

examination,

but anterior to the lateral geniculate might show poor pupillary response but would have a characterRetinal

of

seems an

diagnosis

as occurred later on, then this to be a chiasmal or anterior le-

any lesion

giant cell arteritis

it is even

at the stage of “finger If the pupils

than

unlikely

two key diagnostic

careful visual field testing.

evidence

whether

was seen for her fourth

the lesion

be more

normal

were not provided. help place

symptoms of giant usually is associat-

case to make the diagnosis

particular Finally,

ing” would have been a pupil evaluation

rate, there was no indica-

must

there is in the present

presented to us by the neurologist are very incomplete, and we have to assume that additional data The

might be con-

with an elevated

The data

to have

to a neurologist.

sedimentation

of the

ed with a severe anterior ischemic optic neuropathy. While posterior ischemic optic neuropathy is occasionally

with this case in terms

was made

the

field examination.

patient

as “no

Seven

and started

no mention

and there was no visual

eyes.

to light, but there was a good

ly seen by an optometrist, vision,

biopsy,

sedimentation

sidered

This

response to convergence. There are several problems of the method

57

here.

and one week later

eyes.

about

found to be unreactive

artery

of

she was recorded

in both

light perception”

rate

reported

Next, the patient saw an ophthalmologist who noted vision of “hand motions” and an erythrocyte

The patient produce

weeks.

in both

growing tumor or an inflammatory ly

diagnosis.

when properly intrinsic

Computerized done,

chiasmal

metastatic produce

lymphomas

gliomas

a rapidly

not

lesion is the likescan, to be an

chiasmal

glioma.

meningiomas, or sarcoidosis

may

A biopsy should be taken of

the chiasm which would confirm malignant chiasmal glioma. While

Either

shows what appears

of a malignant

such a picture.

fairly lowgrade,

does

tomographic

craniopharyngiomas, disease,

of visual

disease

lesion (Fig. 2), and this would go

best with a dignosis Occasionally,

examina-

eyes.

progression

this type of progression.

to

that the

lesion, prob-

Fundus

Vascular

fields

to react

indicating

visual pathway

had a stepwise

loss over seven

so visual failed

that occur

the diagnosis

in children

in adults chiasmal

of a

are usually

gliomas

are often

malignant and produce rapidly developing signs and symptoms. Frequently these patients have progressive visual loss with a normal fundus initially, then subsequently develop disc swelling and signs of venous and arterial occlusive disease. Careful examination of the contralateral eye, looking for a junctional scotoma, would be an immediate indication for a CT scan with the possibility for a chiasmal

256

Surv Ophthalmol 30(4) January-February

1986

SLAMOVITS,

BURDE

Fig. 3. Photomicrograph demonstrating bizarre hyperchromatic and pleomorphic astrocytes infiltrating the central nervous system parenchyma.

malignant glioma.‘0*2’ Malignant gliomas of the optic pathways are uncommon in adults and frequently are difficult to diagnose. 7,‘o,20,2’Clinically, these patients always present first with visual symptoms and then with symptoms related to invasion of the hypothalamus and more distant structures, such as the internal capsule, later in the course of the disease.7,‘0 These are aggressively lethal neoplasms which were initially thought to appear in middle-aged men, but now are found to appear also in women. Frequently, retrobulbar pain is present simulating optic neuritis and can confuse the issue early on. Properly performed visual field testing early in the course of the disease will indicate the chiasmal nature of the tumor and lead to the proper diagnostic evaluation. Usually within a matter of several weeks or months, the patient is totally and irrevocably blind in both eyes. lo Death is often said to occur in less than one Thus, progressive visual loss in both eyes, year. 10~20~2’ even with a negative CT scan, means a chiasmal lesion should be considered and a biopsy undertaken.*l Magnetic resonance imaging may help in the future to diagnose these patients. Radiologic appearance is not always completely typical.*’ Barbaro and associates* report a case which had the appearance of a cystic craniopharyngioma or cystic pituitary adenoma but turned out to be a malignant optic glioma. Once the diagnosis is confirmed, radiotherapy and chemotherapy are started, although to date the prognosis for these individuals is extremely

poor. ‘“,‘g,2’ We recently saw a patient with a vascular occlusion in one eye followed by visual loss in that eye. Within several weeks the patient had a superior temporal cut in the other eye. An open biopsy showed a malignant glioma. Chemotherapy and radiotherapy were instituted, and the patient still has vision in her second eye several months later, although prognostically our patient probably has a very dim outlook, similar to the patient presented here. In summary, four practitioners examined the present patient. Had a careful neuro-ophthalmologic examination including visual fields and pupil examination been accomplished early in the course of the illness, it may have been possible to focus on the origin of the pathology and prevent this patient from having to visit four different doctors in order to reach the correct diagnosis. This emphasizes the value of a proper clinical examination and the use of appropriate laboratory tests, such as a CT scan, looking both at the chiasm and the occipital lobe with cuts of the appropriate thickness. The visual evoked response, which occasionally can be helpful, in the wrong hands or improperly interpreted can be totally worthless, as it was in this case. Concluding Comments by Ronald M. Burde, M.D. Doctor Keltner’s cogent comments concerning the inadequacy of the historical information with respect to absence of data about pupillary reactivity and visual fields is worth emphasizing. Surely the

VISUAL

LOSS WITH

diagnosis

NORMAL

could have been made earlier

ate clinical

tests

and

had been performed.

subsequent

Whether

257

EXAMINATION if appropri-

diagnostic

making

tests

the diagnosis

earlier in the course of the disease would have made a difference

is moot. The differential

time of the CT

scan was malignant

central

system

derwent

nervous

a stereotactic

nosis was anaplastic

lymphoma.

diagnosis glioma

The patient

optic tract biopsy. astrocytoma

at the versus

(Fig.

un-

The diag3).

References 1. Baker HL, Berquist TH, Kispert DB, et al: Magnetic resonance imaging in a routine clinical setting. Mayo Clin Proc 60:75-90, 1985 2. Barbaro NM, Rosenblum ML, Maitland GG, et al: Malignant optic glioma presenting radiologically as a “cystic” suprasellar mass. Case report and review of the literature. Neurosurgery 1lt787-789, 1982 3. Bodis-Wollner I, Atkin A, Raab F, Wolkstein M: Visual association cortex and vision in man. Pattern-evoked occipital potentials in a blind boy. Science I98:62%630, 1977 PR: Visual 4. Celesia GG, Archer CR, Kuroiwa Y, Goldfader function ofthe extrageniculo-calcarine system in man. Relationship to cortical blindness. Arch Neural 37:704-706, 1980 of the optic 5. Gibberg FB, Miller RN, Morgan AD: Glioblastoma chiasm. Br J Ophthalmol 57:78&791, 1973 6. Hamilton AM, Garner A, Tripathi RC, Sanders MD: Malignant optic nerve glioma. Report of a case with electron microscopic study. Br J Ophthalmol 57:253-264, 1973 7. Harper CG, Stewart-Wynne EG: Malignant optic gliomas in adults. Arch Neural 35:731-735, 1978 8. Hayreh SS: Posterior ischemic optic neuropathy. Ophthalmologica 182:2%41, 1981 9. Hedges TR III, Gieger GL, Albert DM: The clinical value of negative temporal artery biopsy specimens. Arch Ophthalmol Z01:1251-1254, 1983 10. Hoyt WF, Meshel LG, Lessell S, et al: Malignant optic glioma

of adulthood. Brain 96:121-132, 1973 11. Jayle GE, Tassy J, Deransart-Ferrer0 A, Cornand A: Un cas de cecite corticale avec conservation du potentiel evoque visual occipital. Reu Otoneuroophtalmol 43:22%232, 1971 12. Keltner JL: Giant-cell arteritis. Signs and symptoms. Ophthalmology89:1101-1110, 1982 13. Kupersmith MJ, Siegel IM, Carr RE, et al: Visual evoked potentials in chiasmal gliomas in four adults. Arch Neural 38:362365, 1981 14. Lee KF, Schatz NJ, Savino PJ: Ischemic chiasmal syndrome, in, Glaser JS, Smith JL (ed): Neuro-Ophthalmology. St. Louis, CV Mosby Company, 1975, Vol VIII, pp 115-130 15. Manor RS, Israeli J, Sandbank U: Malignant optic glioma in a 70-year-old patient. Arch Ophthalmol 94:1142-l 144, 1976 16. Mattson RH, Peterson EW: Glioblastoma multiforme of the optic nerve. Report of a case. JAMA 1!%:799-800, 1966 17. Miller NR, Iliff WJ, Green WR: Evaluation and management of gliomas of the anterior visual pathways. Brain 97:743-754, 1974 18. Papo I, Beltrami CA, Salvolini U, Caruselli G: Sarcoidosis sim8:353-355, 1977 ulating a glioma of the optic nerve. Surg Ned 19. Shehata WM, Woodward PM, Budde RB: Optic gliomas, value of preserving vision by radiotherapy. Report of three cases and review of literature. J Ocular Therup Surg 3:262-266, 1984 20. Spoor TC, Kennerdell JS, Martinez AJ, Zorub D: Malignant gliomas of the optic nerve pathways. Am J Ophthalmol 89:284292, 1980 21. Spoor TC, Kennerdell JS, Zorub D, Martinez AJ: Progressive visual loss due to glioblastoma. Normal neuroroentgenographic studies. Arch Neural 38:196-197, 1981 22. Streletz LJ, Bae HO, Roeshman RM, et al: Visual evoked potentials in occipital lobe lesions. Arch Neural 38:80-85, 1981 23. Tang RA, Grotta JC, Lee KF, Lee YE: Chiasmal syndrome in sarcoidosis. Arch Ophthalmol 101:1069-1073, 1983 24. Tychsen L, Hoyt WF: Occipital lobe dysplasia. Arch Ophthalmol 103:680-683, 1985 25. WrightJE, McDonald WI, Call NI: Management ofoptic nerve gliomas. BrJ Ophthalmol 64:545-552, 1980

Reprints

are not available.

Abstract. A 68-year-old woman experienced rapid progressive visual loss to blindness over a seven-week period. Inadequate clinical and diagnostic testing masked the diagnosis of a malig30:251-257, 1986) nant glioma of adulthood. (Surv Ophthalmol

Key words. optic tracts

chiasm

??

hypothalamus

??

lesion

??

malignant glioma

??

optic nerve

??