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Progression of Visual Defects in Ischemic Optic Neuropathy
Progression of Visual Defects in Ischemie Optic Neuropathy Lanning B. K l i n e , M . D .
Six patients with nonarteritic ischemie optic neuropathy experienced worsening of visual acuity and field loss during the six-week peri od after onset (range, three to six weeks), without apparent ophthalmoscopic changes. Thereafter, visual function remained un changed. Various medications were used, but none prevented deterioration of visual func tion. Although not a widely recognized phe nomenon, progression of visual deficit oc curred in these patients in the early weeks after onset of ischemie optic neuropathy.
Case Reports
ISCHEMIC OPTIC NEUROPATHY is characterized by sudden, painless, usually irreversible loss of visual function, an afferent pupillary defect, and optic disk edema. Affected individuals are typically between 45 and 80 years of age. Patho logically, there is ischemic infarction within the laminar portion of the optic nerve. The cause of nonarteritic ischemic optic neuropathy is un certain. About half of affected patients have hypertension, but the remainder lack any spe cific disease. The ophthalmologic literature emphasizes the nonprogressive course of visual loss in ischemic optic neuropathy. 1 6 However, in some patients there is definite deterioration of visual function early in the clinical course. 7 · 8 Herein I describe six patients with progressive visual loss within six weeks of onset of ischemic optic neuropathy. These patients, who ranged in age from 55 to 71 years, were all referred for neuroophthalmic examination. There were three men and three women (Figs. 1 and 2). Two cases are presented in detail.
Casel A 63-year-old woman awoke one morning with a "blurred area" in the superior portion of her right visual field. There was no associated periocular pain or headache, and the patient was taking no medications regularly. One week later she consulted her ophthalmologist, w h o diagnosed right ischemic optic neuropathy. Two weeks after the onset of visual symp toms, visual acuity was R.E.: 20/20 and L.E. 20/15. Results of color vision testing were nor mal in each eye, but there was a right afferent pupillary defect. Eye movements and results of slit-lamp examination were normal. The left visual field was unremarkable, whereas the right visual field showed a superior nerve fiber bundle defect (Fig. 1). The left optic disk was normal, and the right was swollen (Fig. 3). Westergren erythrocyte sedimentation rate was 15 mm/hour. Nine days later (23 days after onset), visual acuity in the right eye had decreased to 20/50; five weeks later it was 20/200. At this time, the patient could no longer recognize any of the Ishihara pseudoisochromatic color plates with the right eye, and the right visual field showed a superior altitudinal defect with involvement of central fixation (Fig. 1). The right optic disk became pale. Results of high resolution computed tomog raphy were normal. After four years of followu p , visual acuity has remained stable at R.E.: 20/200 and L.E.: 20/15.
Accepted for publication May 24, 1988. From the Combined Program in Ophthalmology, Eye Foundation Hospital—University of Alabama in Bir mingham, University of Alabama School of Medicine, Birmingham, Alabama. Reprint requests to Lanning B. Kline, M.D., Suite 555, 1600 7th Ave. S., Birmingham, AL 35233.
Case 4 A 64-year-old woman suddenly lost a portion of the left central visual field. There was no associated pain, and she waited three weeks "hoping it would get better on its own" before consulting an ophthalmologist. At that time, visual acuity was R.E.: 20/25 and L.E.: 20/30. There was a left afferent pupillary defect, a
©AMERICAN JOURNAL OF OPHTHALMOLOGY 106:199-203, AUGUST, 1988
199
200
August, 1988
AMERICAN JOURNAL OF OPHTHALMOLOGY
Patient No., Age, Sex
Initial visual field Time from onset (weeks) Visual acuity
Final visual field Time from onset (weeks) Visual acuity
RE: 20/20
RE: 20/200
1,63, F
2, 71, M
1V2
LE: 20/80
LE: 20/400
3, 55, M
~ "
= | 4 β
2 3 — =V4e RE: 20/25 RE: 20/400 Fig. 1 (Kline). Summary of clinical data and visual fields for Patients 1, 2, and 3. cecocentral scotoma in the left visual field (Fig. 2), and diffuse edema of the left disk. One year previously the patient experienced transient right arm numbness and weakness. She had been taking aspirin and dipyridamole regularly since that time. Westergren sedimentation rate was 30 mm/ hour, and results of complete blood cell count, prothrombin time, partial thromboplastin time, and skull x-rays were normal. Five weeks after onset, visual acuity was R.E.: 20/25 and L.E.: 20/80. The left visual field
showed extensive superior and central loss (Fig. 2). The left disk was swollen, with exudates in the papillomacular bundle. Over the next five months, visual acuity in the left eye remained 20/80 and the left disk became pale.
Discussion Progression of visual loss early in the course of ischemie optic neuropathy has received little
Visual Field Defects in Ischemie Optic Neuropathy
Vol. 106, No. 2
Patient No., Age, Sex
Initial visual field Time from onset (weeks) Visual acuity
Final visual field Time from onset (weeks) Visual acuity
LE: 20/30
5 LE: 20/80
201
4, 64, F
"Ve
^S
f V \ s
5, ββ, F
\ >ί*
ΐϊ^ =ai
1 1 ft \
fui
J j [i a
'^4/T/iì
l<
^e
^è^ /
1ίϊ\.
/li*
V/2
RE: 20/200
RE: 20/30 135/
6, 61, M
/
\«
é^F =3 Λτ5\
flfr
li1
liti
IM V^\f
ÌC^K^
=l4e ™ ~ =V4e
/"'
2ϊϊ^
LE: 20/20
LE:
Finger counting
Fig. 2 (Kline). Summary of clinical data and visual fields for Patients 4, 5, and 6.
attention. Miller and Smith, 1 who first applied the term ischemie optic neuropathy to the clini cal syndrome, described progression of visual loss in one of 11 patients. In their patient, visual acuity decreased from 20/30 to 20/70, but the time course was not discussed. In 1973, Ellenberger, Keltner, and Bürde 3 reported no change in vision in most of their 48 patients, improvement in one third, and deterioration in two patients. No further data were given re garding these last two cases. Clinical progression of ischemie optic neu
ropathy was discussed by Boghen and Glaser 7 in their review of 42 patients. In that series, visual field data were available in 34 patients, 11 (30%) of whom had progressive worsening over a period of several days to four weeks. Two illustrative cases were reported. A 61-yearold man had an initial visual acuity of 20/15 in the right eye, an inferior altitudinal defect, and swelling of only the superior aspect of the right disk. Within three weeks, visual acuity had decreased to counting fingers at 3 feet, with diffuse right optic disk edema. The second
202
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 3 (Kline). Case 1. Diffuse right optic disk edema two weeks after onset of ischemie optic neu ropathy. patient was a 63-year-old man with a visual acuity of 20/20 in the right eye and a swollen disk temporally. Within two weeks, visual acu ity had decreased to counting fingers at 6 feet and the nerve head was diffusely swollen. Shults 8 described a 39-year-old man who de veloped bilateral consecutive ischemie optic neuropathy; visual loss progressed over about one week in each eye. Although there was no mention of progressive loss of visual function in ischemie optic neuropathy in his mono graph, 4 Hayreh 9 has subsequently stated that "visual loss is usually non-progressive, but occasionally may be progressive for several hours or days." Beck and coworkers 10 reported recurrent epi sodes of ischemie optic neuropathy in the same eye. Of the four patients described, three ex perienced visual deterioration from one to three weeks after the initial episode. They all had segmental edema of the superior portion of the disk, which progressed to encompass the inferior aspect as well with concurrent loss of visual acuity and field. The fourth patient, a 52-year-old man, experienced recurrence of dif fuse disk edema 45 months after his initial attack of ischemie optic neuropathy in the same eye. Visual field loss progressed from an inferi or nerve fiber bundle defect to a complete inferior altitudinal defect, and visual acuity decreased from 20/25 to 20/100. The authors believed that their cases represented a second episode of ischemie optic neuropathy that
August, 1988
should be distinguished from progression within a single episode. The patients described herein most closely resemble those described by Boghen and Gla ser 7 and Shults. 8 They all initially had a swollen disk on the involved side and had decreasing visual acuity and progression of their field defect within six weeks after onset of the initial episode. There were no apparent ophthalmoscopic changes during the period of visual decline, nor any clues that progression might occur. Shults 8 emphasized the difficulty in as sessing visual function using ophthalmoscopy. Two patients in this study (Cases 2 and 3) were unaware of further loss of vision. In four cases (Cases 1, 3, 5, and 6), initial field loss was characterized by a nerve fiber bundle defect, and with progression to involve the papillomacular bundle, there was an associated de cline in visual acuity. Cecocentral scotomas, the initial manifestation in two patients, subse quently progressed to involve either the superi or (Case 4) or inferior (Case 2) field. No patients in the present series, nor in any previously reported with clinical progression, were found to have giant cell arteritis. Rather, all were believed to have the arteriosclerotic form of ischemie optic neuropathy. The origin of clinical progression in ischemie optic neuropathy is unknown. Its basis may lie in the dissociation observed in ischemie optic neuropathy between the appearance of optic disk edema and decline in visual function. Boghen and Glaser 7 described a 63-year-old woman who had simultaneous bilateral disk swelling, yet noted acute loss of vision only in the right eye. Two weeks later, vision decreased rapidly in the left eye. Hayreh 11 described four patients with ischemie optic neuropathy in whom optic disk edema preceded loss of visual acuity or field by two weeks to seven months. Six other patients have been described with asymptomatic optic disk edema that pro gressed to sudden visual loss after three days (one case), 12 two to six months (four cases), 13 and at a later date (one case). 14 There appears to be a spectrum in the onset of visual loss in ischemie optic neuropathy (Fig. 4). Hayreh 11 speculated that this may be related to the de gree of optic disk ischemia. Thus, in eyes with ischemie optic neuropathy and preserved cen tral visual acuity, ischemia causes only optic disk edema because of axoplasmic flow stasis. In more severe instances, ischemia also inter feres with visual impulse transmission, with a corresponding loss of visual acuity. A variety of treatment modalities have failed to prevent progression of visual loss in ische-
Visual Field Defects in Ischemie Optic Neuropathy
Vol. 106, No. 2
20/20 -
203
TY
VISUAL ACUITY
NLP
*
-//-
Fig. 4 (Kline). Three differ ent patterns of visual loss that may occur with an epi sode of ischemie optic neu ropathy. NLP, no light per ception.
+
TIME (months)
A = abrupt, non prog ressi ve visual loss B = initial mild visual loss with progression up to 6 weeks C = abrupt visual decline between 1-7 months mie optic neuropathy. One patient described by Boghen and Glaser 7 was treated with three retrobulbar injections of corticosteroids, and another was already anticoagulated (warfarin). Three of the patients in this study were being treated with platelet antiaggregants (aspirin or dypyridamole), one with a beta-blocker (propranolol), and one with systemic corticoste roids (prednisone). At this time, there is no medication known to prevent this progressive course. Awareness of the potential for visual worsen ing in ischemie optic neuropathy will eliminate unnecessary patient examination. Three pa tients in the present series underwent radiographic examinations (skull x-rays and cranial computed tomography), one underwent carot id Doppler studies, and one, a temporal artery biopsy, despite lack of symptoms suggestive of giant cell arteritis and a Westergren erythrocyte sedimentation rate of 2 mm/hour. The ophthalmologist should use caution in relaying information regarding visual progno sis to a patient with ischemie optic neuropathy. It seems prudent to defer making a prognosis until six weeks after onset of visual loss.
References 1. Miller, G. R., and Smith, J. L.: Ischemie optic neuropathy. Am. J. Ophthalmol. 62:103, 1966. 2. Cullen, J. F.: Ischemie optic neuropathy. Trans. Ophthalmol. Soc. U.K. 897:759, 1967. 3.' Ellenberger, C , Keltner, J. L., and Bürde,
R. M : Acute optic neuropathy in older patients. Arch. Ophthalmol. 28:182, 1973. 4. Hayreh, S. S.: Anterior Ischemie Optic Neurop athy. New York, Springer-Verlag Publishing Co., Inc., 1975. 5. Repka, M. X., Savino, P. J., Schatz, N. J., and Sergott, R. C : Clinical profile and long-term implica tions of anterior ischemie optic neuropathy. Am. J. Ophthalmol. 96:478, 1983. 6. Bürde, R. M., Savino, P. J., and Trobe, J. D.: Clinical Decisions in Neuro-ophthalmology. St. Louis, C. V. Mosby, 1985, chap. 1, pp.41-46. 7. Boghen, D. R., and Glaser, J. S.: Ischemie optic neuropathy. The clinical profile and natural history. Brain 98:689, 1975. 8. Shults, W. T.: Ischemie optic neuropathy. Some interesting features. Trans. Pac. Coast Otoophthalmol. Soc. 58:281, 1977. 9. Hayreh, S. S.: Anterior ischemie optic neuropa thy. Arch. Neurol. 38:675, 1981. 10. Beck, R. W., Savino, P. J., Schatz, N. J., Smith, C. H., and Sergott, R.: Anterior ischemie optic neuropathy. Recurrent episodes in the same eye. Br. J. Ophthalmol. 67:705, 1983. 11. Hayreh, S. S.: Anterior ischemie optic neurop athy. V. Optic disc edema an early sign. Arch. Ophthalmol. 99:1030, 1981. 12. Sanders, M. D.: Ischemie papillopathy. Trans. Ophthalmol. Soc. U.K. 91:369, 1971. 13. Geordiades, G., Kanstas, P., and Stanges, N.: Reflections issues d l'etude de numbreux case de pseudo-papillite vasculaire. Bull. Soc. Fr. Ophtalmol. 79:506, 1966. 14. Foulds, W. S.: Ischaemic optic neuropathy. In Cart, J. (ed.): Proceedings of the William Mackenzie Courtenay Symposium in the Ocular Circulation in Health and Disease. London, Henry Kimpton, 1968, pp. 136-141.
Six patients with nonarteritic ischemie optic neuropathy experienced worsening of visual acuity and field loss during the six-week peri od after onset (range, three to six weeks), without apparent ophthalmoscopic changes. Thereafter, visual function remained un changed. Various medications were used, but none prevented deterioration of visual func tion. Although not a widely recognized phe nomenon, progression of visual deficit oc curred in these patients in the early weeks after onset of ischemie optic neuropathy.
Case Reports
ISCHEMIC OPTIC NEUROPATHY is characterized by sudden, painless, usually irreversible loss of visual function, an afferent pupillary defect, and optic disk edema. Affected individuals are typically between 45 and 80 years of age. Patho logically, there is ischemic infarction within the laminar portion of the optic nerve. The cause of nonarteritic ischemic optic neuropathy is un certain. About half of affected patients have hypertension, but the remainder lack any spe cific disease. The ophthalmologic literature emphasizes the nonprogressive course of visual loss in ischemic optic neuropathy. 1 6 However, in some patients there is definite deterioration of visual function early in the clinical course. 7 · 8 Herein I describe six patients with progressive visual loss within six weeks of onset of ischemic optic neuropathy. These patients, who ranged in age from 55 to 71 years, were all referred for neuroophthalmic examination. There were three men and three women (Figs. 1 and 2). Two cases are presented in detail.
Casel A 63-year-old woman awoke one morning with a "blurred area" in the superior portion of her right visual field. There was no associated periocular pain or headache, and the patient was taking no medications regularly. One week later she consulted her ophthalmologist, w h o diagnosed right ischemic optic neuropathy. Two weeks after the onset of visual symp toms, visual acuity was R.E.: 20/20 and L.E. 20/15. Results of color vision testing were nor mal in each eye, but there was a right afferent pupillary defect. Eye movements and results of slit-lamp examination were normal. The left visual field was unremarkable, whereas the right visual field showed a superior nerve fiber bundle defect (Fig. 1). The left optic disk was normal, and the right was swollen (Fig. 3). Westergren erythrocyte sedimentation rate was 15 mm/hour. Nine days later (23 days after onset), visual acuity in the right eye had decreased to 20/50; five weeks later it was 20/200. At this time, the patient could no longer recognize any of the Ishihara pseudoisochromatic color plates with the right eye, and the right visual field showed a superior altitudinal defect with involvement of central fixation (Fig. 1). The right optic disk became pale. Results of high resolution computed tomog raphy were normal. After four years of followu p , visual acuity has remained stable at R.E.: 20/200 and L.E.: 20/15.
Accepted for publication May 24, 1988. From the Combined Program in Ophthalmology, Eye Foundation Hospital—University of Alabama in Bir mingham, University of Alabama School of Medicine, Birmingham, Alabama. Reprint requests to Lanning B. Kline, M.D., Suite 555, 1600 7th Ave. S., Birmingham, AL 35233.
Case 4 A 64-year-old woman suddenly lost a portion of the left central visual field. There was no associated pain, and she waited three weeks "hoping it would get better on its own" before consulting an ophthalmologist. At that time, visual acuity was R.E.: 20/25 and L.E.: 20/30. There was a left afferent pupillary defect, a
©AMERICAN JOURNAL OF OPHTHALMOLOGY 106:199-203, AUGUST, 1988
199
200
August, 1988
AMERICAN JOURNAL OF OPHTHALMOLOGY
Patient No., Age, Sex
Initial visual field Time from onset (weeks) Visual acuity
Final visual field Time from onset (weeks) Visual acuity
RE: 20/20
RE: 20/200
1,63, F
2, 71, M
1V2
LE: 20/80
LE: 20/400
3, 55, M
~ "
= | 4 β
2 3 — =V4e RE: 20/25 RE: 20/400 Fig. 1 (Kline). Summary of clinical data and visual fields for Patients 1, 2, and 3. cecocentral scotoma in the left visual field (Fig. 2), and diffuse edema of the left disk. One year previously the patient experienced transient right arm numbness and weakness. She had been taking aspirin and dipyridamole regularly since that time. Westergren sedimentation rate was 30 mm/ hour, and results of complete blood cell count, prothrombin time, partial thromboplastin time, and skull x-rays were normal. Five weeks after onset, visual acuity was R.E.: 20/25 and L.E.: 20/80. The left visual field
showed extensive superior and central loss (Fig. 2). The left disk was swollen, with exudates in the papillomacular bundle. Over the next five months, visual acuity in the left eye remained 20/80 and the left disk became pale.
Discussion Progression of visual loss early in the course of ischemie optic neuropathy has received little
Visual Field Defects in Ischemie Optic Neuropathy
Vol. 106, No. 2
Patient No., Age, Sex
Initial visual field Time from onset (weeks) Visual acuity
Final visual field Time from onset (weeks) Visual acuity
LE: 20/30
5 LE: 20/80
201
4, 64, F
"Ve
^S
f V \ s
5, ββ, F
\ >ί*
ΐϊ^ =ai
1 1 ft \
fui
J j [i a
'^4/T/iì
l<
^e
^è^ /
1ίϊ\.
/li*
V/2
RE: 20/200
RE: 20/30 135/
6, 61, M
/
\«
é^F =3 Λτ5\
flfr
li1
liti
IM V^\f
ÌC^K^
=l4e ™ ~ =V4e
/"'
2ϊϊ^
LE: 20/20
LE:
Finger counting
Fig. 2 (Kline). Summary of clinical data and visual fields for Patients 4, 5, and 6.
attention. Miller and Smith, 1 who first applied the term ischemie optic neuropathy to the clini cal syndrome, described progression of visual loss in one of 11 patients. In their patient, visual acuity decreased from 20/30 to 20/70, but the time course was not discussed. In 1973, Ellenberger, Keltner, and Bürde 3 reported no change in vision in most of their 48 patients, improvement in one third, and deterioration in two patients. No further data were given re garding these last two cases. Clinical progression of ischemie optic neu
ropathy was discussed by Boghen and Glaser 7 in their review of 42 patients. In that series, visual field data were available in 34 patients, 11 (30%) of whom had progressive worsening over a period of several days to four weeks. Two illustrative cases were reported. A 61-yearold man had an initial visual acuity of 20/15 in the right eye, an inferior altitudinal defect, and swelling of only the superior aspect of the right disk. Within three weeks, visual acuity had decreased to counting fingers at 3 feet, with diffuse right optic disk edema. The second
202
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 3 (Kline). Case 1. Diffuse right optic disk edema two weeks after onset of ischemie optic neu ropathy. patient was a 63-year-old man with a visual acuity of 20/20 in the right eye and a swollen disk temporally. Within two weeks, visual acu ity had decreased to counting fingers at 6 feet and the nerve head was diffusely swollen. Shults 8 described a 39-year-old man who de veloped bilateral consecutive ischemie optic neuropathy; visual loss progressed over about one week in each eye. Although there was no mention of progressive loss of visual function in ischemie optic neuropathy in his mono graph, 4 Hayreh 9 has subsequently stated that "visual loss is usually non-progressive, but occasionally may be progressive for several hours or days." Beck and coworkers 10 reported recurrent epi sodes of ischemie optic neuropathy in the same eye. Of the four patients described, three ex perienced visual deterioration from one to three weeks after the initial episode. They all had segmental edema of the superior portion of the disk, which progressed to encompass the inferior aspect as well with concurrent loss of visual acuity and field. The fourth patient, a 52-year-old man, experienced recurrence of dif fuse disk edema 45 months after his initial attack of ischemie optic neuropathy in the same eye. Visual field loss progressed from an inferi or nerve fiber bundle defect to a complete inferior altitudinal defect, and visual acuity decreased from 20/25 to 20/100. The authors believed that their cases represented a second episode of ischemie optic neuropathy that
August, 1988
should be distinguished from progression within a single episode. The patients described herein most closely resemble those described by Boghen and Gla ser 7 and Shults. 8 They all initially had a swollen disk on the involved side and had decreasing visual acuity and progression of their field defect within six weeks after onset of the initial episode. There were no apparent ophthalmoscopic changes during the period of visual decline, nor any clues that progression might occur. Shults 8 emphasized the difficulty in as sessing visual function using ophthalmoscopy. Two patients in this study (Cases 2 and 3) were unaware of further loss of vision. In four cases (Cases 1, 3, 5, and 6), initial field loss was characterized by a nerve fiber bundle defect, and with progression to involve the papillomacular bundle, there was an associated de cline in visual acuity. Cecocentral scotomas, the initial manifestation in two patients, subse quently progressed to involve either the superi or (Case 4) or inferior (Case 2) field. No patients in the present series, nor in any previously reported with clinical progression, were found to have giant cell arteritis. Rather, all were believed to have the arteriosclerotic form of ischemie optic neuropathy. The origin of clinical progression in ischemie optic neuropathy is unknown. Its basis may lie in the dissociation observed in ischemie optic neuropathy between the appearance of optic disk edema and decline in visual function. Boghen and Glaser 7 described a 63-year-old woman who had simultaneous bilateral disk swelling, yet noted acute loss of vision only in the right eye. Two weeks later, vision decreased rapidly in the left eye. Hayreh 11 described four patients with ischemie optic neuropathy in whom optic disk edema preceded loss of visual acuity or field by two weeks to seven months. Six other patients have been described with asymptomatic optic disk edema that pro gressed to sudden visual loss after three days (one case), 12 two to six months (four cases), 13 and at a later date (one case). 14 There appears to be a spectrum in the onset of visual loss in ischemie optic neuropathy (Fig. 4). Hayreh 11 speculated that this may be related to the de gree of optic disk ischemia. Thus, in eyes with ischemie optic neuropathy and preserved cen tral visual acuity, ischemia causes only optic disk edema because of axoplasmic flow stasis. In more severe instances, ischemia also inter feres with visual impulse transmission, with a corresponding loss of visual acuity. A variety of treatment modalities have failed to prevent progression of visual loss in ische-
Visual Field Defects in Ischemie Optic Neuropathy
Vol. 106, No. 2
20/20 -
203
TY
VISUAL ACUITY
NLP
*
-//-
Fig. 4 (Kline). Three differ ent patterns of visual loss that may occur with an epi sode of ischemie optic neu ropathy. NLP, no light per ception.
+
TIME (months)
A = abrupt, non prog ressi ve visual loss B = initial mild visual loss with progression up to 6 weeks C = abrupt visual decline between 1-7 months mie optic neuropathy. One patient described by Boghen and Glaser 7 was treated with three retrobulbar injections of corticosteroids, and another was already anticoagulated (warfarin). Three of the patients in this study were being treated with platelet antiaggregants (aspirin or dypyridamole), one with a beta-blocker (propranolol), and one with systemic corticoste roids (prednisone). At this time, there is no medication known to prevent this progressive course. Awareness of the potential for visual worsen ing in ischemie optic neuropathy will eliminate unnecessary patient examination. Three pa tients in the present series underwent radiographic examinations (skull x-rays and cranial computed tomography), one underwent carot id Doppler studies, and one, a temporal artery biopsy, despite lack of symptoms suggestive of giant cell arteritis and a Westergren erythrocyte sedimentation rate of 2 mm/hour. The ophthalmologist should use caution in relaying information regarding visual progno sis to a patient with ischemie optic neuropathy. It seems prudent to defer making a prognosis until six weeks after onset of visual loss.
References 1. Miller, G. R., and Smith, J. L.: Ischemie optic neuropathy. Am. J. Ophthalmol. 62:103, 1966. 2. Cullen, J. F.: Ischemie optic neuropathy. Trans. Ophthalmol. Soc. U.K. 897:759, 1967. 3.' Ellenberger, C , Keltner, J. L., and Bürde,
R. M : Acute optic neuropathy in older patients. Arch. Ophthalmol. 28:182, 1973. 4. Hayreh, S. S.: Anterior Ischemie Optic Neurop athy. New York, Springer-Verlag Publishing Co., Inc., 1975. 5. Repka, M. X., Savino, P. J., Schatz, N. J., and Sergott, R. C : Clinical profile and long-term implica tions of anterior ischemie optic neuropathy. Am. J. Ophthalmol. 96:478, 1983. 6. Bürde, R. M., Savino, P. J., and Trobe, J. D.: Clinical Decisions in Neuro-ophthalmology. St. Louis, C. V. Mosby, 1985, chap. 1, pp.41-46. 7. Boghen, D. R., and Glaser, J. S.: Ischemie optic neuropathy. The clinical profile and natural history. Brain 98:689, 1975. 8. Shults, W. T.: Ischemie optic neuropathy. Some interesting features. Trans. Pac. Coast Otoophthalmol. Soc. 58:281, 1977. 9. Hayreh, S. S.: Anterior ischemie optic neuropa thy. Arch. Neurol. 38:675, 1981. 10. Beck, R. W., Savino, P. J., Schatz, N. J., Smith, C. H., and Sergott, R.: Anterior ischemie optic neuropathy. Recurrent episodes in the same eye. Br. J. Ophthalmol. 67:705, 1983. 11. Hayreh, S. S.: Anterior ischemie optic neurop athy. V. Optic disc edema an early sign. Arch. Ophthalmol. 99:1030, 1981. 12. Sanders, M. D.: Ischemie papillopathy. Trans. Ophthalmol. Soc. U.K. 91:369, 1971. 13. Geordiades, G., Kanstas, P., and Stanges, N.: Reflections issues d l'etude de numbreux case de pseudo-papillite vasculaire. Bull. Soc. Fr. Ophtalmol. 79:506, 1966. 14. Foulds, W. S.: Ischaemic optic neuropathy. In Cart, J. (ed.): Proceedings of the William Mackenzie Courtenay Symposium in the Ocular Circulation in Health and Disease. London, Henry Kimpton, 1968, pp. 136-141.