Treatment of Traumatic Optic Neuropathy With Corticosteroids Thomas C. Spoor, M.D., Walter C. Hartel, M.D., Daniel B. Lensink, M.D., and Michael J. Wilkinson, M.D. We treated 21 patients (22 eyes) with traumatic optic neuropathy by using intravenous megadose methylprednisolone (13 patients) or high-dose dexamethasone (eight patients). Of 13 patients treated with megadose methylprednisolone, 12 had improved visual function, as did seven of nine eyes treated with intravenous dexamethasone. This difference was not significant (P = .3). Initial total blindness, mechanism of injury, or time from injury to treatment did not correlate with visual improvement. LITTLE AGREEMENT exists as to appropriate treatment of patients with optic nerve injuries after craniofacial trauma. Treatment options include observation.' corticosteroids," corticosteroids and osmotic agents," and surgery to decompress the optic canal.v' We successfully treated patients with traumatic optic neuropathy by using intravenous high-dose and megadose corticosteroids.
Patients and Methods Traumatic optic neuropathy is defined as traumatic visual loss that occurs in the presence of an afferent pupillary defect without evidence of injury to the eye or optic nerve.Y Patients with such neuropathies were examined and treated at two trauma centers (Miami Valley Hospital, Dayton, Ohio and Kresge Eye Institute, Detroit Receiving Hospital, Detroit, Michigan). All patients received a complete neuroAccepted for publication Aug. 27, 1990. From the Kresge Eye Institute, Wayne State University, Detroit, Michigan (Drs. Spoor, Lensink, and Wilkinson); and Department of Ophthalmology, Wright State University School of Medicine, Dayton, Ohio (Dr. Hartel). Reprint requests to Thomas C. Spoor, M.D., F.A.C.S., Kresge Eye Institute, Wayne State University, 4717 St. Antoine, Detroit, MI 48201.
©AMERICAN JOURNAL OF OPHTHALMOLOGY
110:665-669,
ophthalmic examination and high-resolution computed tomography of the brain and orbits, including bone window images. Patients with associated concussive or penetrating ocular injuries were excluded from the study. Eight patients (Dayton) were treated with intravenous dexamethasone, 20.0 mg every six hours (approximately 0.25 mg Zkg of body weight for 48 hours). Thirteen patients (Detroit) were treated with intravenous methylprednisolone, 30.0 mg Zkg of body weight initially, followed two hours later by 15.0 mg/kg of body weight every six hours for 48 hours. In both groups, corticosteroids were tapered rapidly after 48 hours. The time between injury and initiation of treatment was variable, ranging from 8th hours to 15 days (mean, 4.2 days) in the group treated with intravenous methylprednisolone. Treatment with intravenous dexamethasone was initiated earlier (four hours to four days; mean, 17 hours). Seventeen patients were male and four patients were female. Motor vehicle accidents accounted for most of the injuries (ten), followed closely by assaults (eight) and falls (three). The assault group contained three patients with penetrating orbital injuries, two caused by knives and one caused by a BB pellet. These patients were included since eventual visual and motility recovery indicated that the apical orbital structures had not been transsected.
Results Thirteen patients were treated with intravenous megadoses of methylprednisolone (Tables 1 and 2), and eight patients were treated with high doses of intravenous dexamethasone (Tables 3 and 4). Patients treated with methylprednisolone received much higher doses of corticosteroids than those treated with dexamethasone (20 times the initial dose and ten DECEMBER,
1990
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666
December, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
TABLE 1 CHARACTERISTICS OF PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY TREATED WITH MEGADOSE CORTICOSTEROIDS' CASE NO., SEX
INJURY TO
VISUAL ACUITY'
AGE (VRS), INITIAL
POSTPULSE
TRAUMA
TREATMENT FINAL
INTERVAL
FOLLOW-UP
CAUSE
INJURY
1,33, M NLP
NLP
NLP
2 days
3 weeks
Fall from truck
Optic canal
2,21, M 20/200
20/40
20/25
15 days
1 month
3,38, M HM 4.27, M 20/40 5.15, M 20/200
20/70 20/20 20/30
20/30 20/20 20/30
8 hours 7 days 8 days
2 weeks 6 weeks 6 months
Trimalar fracture. epidural hematoma Trirnalar fracture
6,31, M NLP
20/200
20/100
2'12 days
3 years
Motor vehicle accident Baseball bat Wrench to head Bike hit by train Knife to orbit
7,27, M NLP
NLP
20/50
2 days
1 week
8,25, M 20/200 9,40, M LP
20/20 20/400
20/20 20/25
24 hours 2 hours
10. 16, M HM
20/200
20/50
3 days
11,30. F
20/400
20/100
20/50
20 hours
12, 28. F
CF
20/400
20/30
12 hours
20/40
20/25
7 days
8 months Fist to face 2 112 months Motor vehicle accident 3 years BB to orbital apex 21/2 months Motor vehicle accident 3 weeks Gun shot wound to the orbit 2 months Fell and struck head
13,38, M 20/80
Knife up nose to orbit
Orbital roof and frontal fractures Pneumocephalus. orbital apex syndrome Orbital apex syndrome
COMMENT
Transcranial optic canal decompression, no improvement
Concomitant orbital apex syndrome resolved Transethmoidal canal decompression after corticosteroid failure
Orbital roof fracture
Transethmoidal decompression Facial fractures Orbital hemorrhage
Canthotomy, cantholysis before corticosteroids
Orbital roof fracture
'Patients treated with methylprednisolone, 30 mg/kg of body weight pulse. then 15 mg/kg of body weight every six hours. tNLP indicates no light perception; HM indicates hand motions; and CF indicates counting fingers,
times the subsequent doses). Most of the patients in both groups had marked improvement in visual function. No statistically significant difference was found between the two groups in final visual improvement (P = .3, chi-square test). Of eight patients treated with intravenous dexamethasone, seven of nine eyes had improved visual function. Of 13 patients treated with megadoses of intravenous methylprednisolone, 12 showed improved visual function. The interval between injury and initiation of treatment was variable. A long interval (mean, 4.2 days) between injury and treatment did not preclude improvement in visual function in most patients treated with megadose methylprednisolone. Few patients treated with highdose dexamethasone demonstrated dramatic visual recovery during treatment despite a
much shorter interval between injury and treatment (mean, 17 hours). Of 13 patients treated with megadose methylprednisolone, 11 had significantly improved visual function within 96 hours after the initiation of treatment. Only two of nine eyes in the group treated with dexamethasone demonstrated this rapid improvement in visual function. This difference was significant (P = .008). Three patients in the mega dose methylprednisolone group underwent subsequent surgical decompression of their optic canal by either a trans cranial (Case 1) or a transethmoidal route (Cases 7 and 10). The patient in Case 1 had an optic canal fracture on computed tomographic scans and an equivocal history of progressive visual loss to no light perception. Another patient (Case 10) had a BB pellet compressing the
Vol. 110, No.6
Traumatic Optic Neuropathy and Corticosteroids
TABLE 2 RESIDUAL VISUAL FIELD DEFECTS IN PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY'
CASE NO.
1 2 3 4 5
6 7
8
9
VISUAL ACUITY' INITIAL
NLP 20/200 HM 20/40
FINAL
NLP 20/25 20/30 20/20
VISUAL FIELD DEFECTS INITIAL
HM
11
20/400 20/50
12 13
CF 20/80
20/50
20/30 20/25
as lessening of central scotomas, sparing fixation, and increased peripheral field (Cases 5, 8, 11, and 13; Tables 2 and 4). Final visual fields, available on 15 eyes, demonstrated varying degrees of central and peripheral visual field loss (Tables 2 and 4).
FINAL
Discussion
Relative central scotoma 20/200 20/30 Superotemporal involving fixation NLP 20/100 NLP NLP 20/50 NLP 20/200 20/20 Inferonasal defect involving fixation LP 20/25 LP
10
667
Full
Superotemporal sparing fixation Inferior altitudinal Superior altitudinal Inferonasal defect sparing fixation Relative central scotoma. peripheral constriction Relative central HM scotoma, peripheral constriction Inferior altitudinal Relative central ininvolving fixation feronasal defect
Dense central sco- Relative central toma, peripheral scotoma, periphconstriction eral constriction
'Patients treated with methylprednisolone. 30 mg/kg of body weight pulse, then 15 mg/kg of body weight every six hours. tNLP indicates no light perception; LP indicates light perception; HM indicates hand motions; and CF indicates counting fingers.
optic nerve at the orbital apex and a medial optic canal fracture. Visual acuity improved from hand motions to 20/200 after intravenous methylprednisolone and subsequently improved to 20/50 after surgery. The visual acuity of one patient (Case 7) was no light perception after five days of intravenous methylprednisolone and improved to 20/50 after transethmoidal optic canal decompression." Initial visual acuity was worse than 20/200 in 20 eyes and totally blind with no light perception in eight eyes. Five of these eight eyes regained some visual function after treatment (Tables 2 and 4). Most patients were too critically injured or vision was too poor to obtain pretreatment visual fields. Visual fields were obtained before and after treatment in only five patients. Visual field improvement was defined
No consensus exists as to the appropriate treatment for patients with traumatic optic neuropathy. Lessell recently reported that only five of 25 untreated patients with indirect optic nerve injuries had improved visual function. Only one of four patients treated with low-dose corticosteroids had improved vision, whereas three of four patients treated with a combination of corticosteroids and trans ethmoidal optic canal decompression showed improvement in visual function. Of our 21 patients treated with intravenous corticosteroids, 17 had improved visual function. Many of our patients with improved visual acuity had residual visual field defects (Tables 2 and 4). When given within eight hours of injury, megadose corticosteroids have been shown to reduce paralysis and other disabilities but do not obviate neurologic deficits in patients with spinal cord injuries." The proposed mechanism is reduction of swelling in the injured tissue and prevention of cell degeneration. Large doses of methylprednisolone slow this degenerative process and increase the blood supply to the injured area, which decreases cell damage secondary to ischemia and hypoxemia." Possibly the corticosteroids decrease intraneural or extraneural edema and compression on the nerve fibers, increasing blood flow and salvaging some of the many nerve fibers subserving central visual acuity. This mechanism would explain the marked improvement in visual acuity and concomitant dense residual visual field defects found in some of our patients. Dosing schedules for high-dose corticosteroid therapy in the treatment of central nervous system trauma vary widely. Reported doses for dexamethasone range from 0.7 to 3.0 mg/kg of body weight, whereas methylprednisolone dosage schedules range from 0.6 to 30.0 mg Zkg of body weight. For the treatment of traumatic optic neuropathy, Anderson, Panje, and Gross" used dexamethasone in loading doses ranging from 16.0 to 60.0 mg followed by doses in the range of 20.0 mg every six hours.
668
December, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
TABLE 3 CHARACTERISTICS OF PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY TREATED WITH HIGH-DOSE CORTICOSTEROIDS' CASE NO., SEX
INJURY TO
VISUAL ACUITY'
AGE (VAS), INITIAL
POSTPULSE
TRAUMA
TREATMENT FINAL
INTERVAL
FOLLOW-UP
CAUSE
Motor vehicle accident Motor vehicle accident Motor vehicle accident Motor vehicle accident Motor vehicle accident Head pinned Hit with tool Motor vehicle accident Fell 2 stories
1,58, M
20/200
20/40
20/20
6 hours
11 months
2,17, M
NLP
NLP
20/30
5 hours
12 months
3,30, F
NLP
LP
20/300
6 hours
6 months
NLP
NLP
NLP
6 hours
6 months
4,18, M
NLP
NLP
NLP
5 hours
2 weeks
5,35, M 6,26, M 7,28, M
NLP LP HM
CF at 3 feet LP HM
20/25 HM CF at 4 feet
4 hours 4 days 7 hours
8 months 6 weeks 5 weeks
8.19, M
20/800
20/25
20/25
9 hours
2 months
INJURY
LeFort III fracture Closed head injury, pneumocephalus
Multiple orbital fracture
Skull fracture Orbit floor and maxilla fracture
'Patients treated with dexamethasone, 20 mg/kg of body weight every six hours. tNLP indicates no light perception; HM indicates hand motions; and CF indicates counting fingers.
Our rationale for using mega dose methylprednisolone to treat traumatic optic neuropathy is based largely on the work done by Braughler and Hall." They maintained that massive doses of corticosteroids (dexamethasone, 6,0 mg/kg of body weight, and methylprednisolone, 30.0 mg/kg of body weight) exhibit a different pharmacologic effect than the standard dose's glucocorticosteroid effect, They cited several examples of both experimental and clinical evidence demonstrating a sharp dose-response curve for methylprednisolone in massive-dose ranges. They believe, based on pharmacokinetics, that methylprednisolone, 30,0 mg zkg of body weight, should be given as soon as possible after injury, followed two hours later and every six hours after that by a dose of 15.0 mg Zkg of body weight. Our patients treated with the megadose methylprednisolone regimen improved much more quickly than those treated with high-dose dexamethasone (P = .008). However, initial visual acuity was not comparable, with a predominance of totally blind eyes (three eyes with light perception) in the dexamethasone group. Final visual results were not significantly different between the two groups (P = .3). Treatment with intravenous corticosteroids seemed to im-
prove visual prognosis whether administered in high doses or megadoses. Two of six totally blind untreated eyes in the TABLE 4 RESIDUAL VISUAL FIELD DEFECTS IN PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY'
CASE NO.
VISUAL FIELD DEFECTS
VISUAL ACUITY' INITIAL
FINAL
1 20/200 20/20 2 NLP 20/30 3 NLP 20/300 NLP NLP 4 NLP NLP 5 NLP 20/25 HM 6 LP CF at 4 feet 7 HM 8 20/800 20/25
INITIAL
FINAL
NLP NLP NLP NLP NLP
Peripheral constriction Temporal and peripheral loss Nasal peripheral loss Relative central scotoma NLP Inferonasal residual island of vision only
Nasal peripheral loss
'Patients treated with dexamethasone. 20 mg/kg of body weight every six hours. tNLP indicates no light perception; LP indicates light perception; HM indicates hand motions; and CF indicates counting fingers.
Vol. 110, No.6
Traumatic Optic Neuropathy and Corticosteroids
series described by Lessell? regained visual acuity of counting fingers and 10/200. Wolin and Lavin" described four patients who recovered vision after total blindness. Three of these patients were treated with corticosteroids, and visual acuity in one patient improved spontaneously. We agree with Wolin and Lavin!' in questioning the role of surgical decompression of the optic canal in patients with sudden, total visual loss. Of our patients, seven (eight eyes) had an initial visual acuity of no light perception after injury. Five of these eyes regained significant visual function after corticosteroid therapy. Visual acuity in two patients improved to better than 20/20 and 20/25, and visual acuity in two other patients improved to 20/ 100 and 20/300. An additional patient did not respond to megadose corticosteroids but did respond to transethmoidal optic canal decempression." Visual acuity in three other eyes remained no light perception despite high-dose dexamethasone (Cases 2 and 3, Table 3) and megadose methylprednisolone followed by transcranial optic canal decompression (Case 1, Table 1). Sudden total blindness does not preclude recovery of visual function and should not rule out corticosteroid treatment. Although most patients had indirect injury to the optic nerves related to facial fractures, some patients received direct, apparently penetrating optic nerve injuries that resulted in total blindness (Cases 6 and 7, Table 1). One patient recovered useful vision after treatment with mega dose corticosteroids. The other patient did not respond to megadose corticosteroids but did recover useful vision after trans ethmoidal optic canal decompression. We cannot predict which injured optic nerves will improve with corticosteroid treatment. We believe that a short course of high-dose or megadose corticosteroids may be useful for patients with traumatic optic neuropathy. The mechanism of injury should not preclude a response to corticosteroid therapy unless obvious avulsion or transsection of the optic nerve is apparent on examination or on computed tomographic scans. Our data are uncontrolled
669
but suggest that high doses of intravenous corticosteroids may help restore vision in patients with traumatic optic neuropathy.
References 1. Hughes, B.: Indirect injury to the optic nerves and chiasm. Bull. Johns Hopkins Hosp. 111:98, 1962. 2. Anderson, R. 1., Panje, W. R., and Gross, C. E.: Optic nerve blindness following blunt forehead trauma. Ophthalmology 89:445, 1982. 3. Matsuzaki, H., Kitahara, K., Kawai, K., and Kumita, M.: The nonsurgical treatment for damage to the intracanalicular portion of the optic nerve. In Highlights in Neuro-Ophthalmology. Proceedings of the International Neuro-Ophthalmology Society, Hakone, Japan. Amsterdam, Aeolus Press, 1987, pp. 27-35. 4. Fukado, Y.: Results in 400 cases of surgical decompression of the optic nerve. Mod. Prob. Ophthalmol. 14:478, 1975. 5. Fugitani, T., Inoue, K., and Takahashi, T.: Indirect traumatic optic neuropathy. Visual outcome of operative and non operative cases. Ipn. J. Ophthalmol. 30:125, 1986. 6. Walsh, F. B., and Hoyt, W. F.: Clinical NeuroOphthalmology, vol. 3, ed. 3. Baltimore, Williams and Wilkins, 1969, p. 2376. 7. Lessell, S.: Indirect optic nerve trauma. Arch. Ophthalmol. 107:382, 1989. 8. Spoor, T. C., and Mathog, R.: Restoration of vision after optic canal decompression following five days of total blindness and mega dose corticosteroid therapy. Arch. Ophthalmol. 104:804, 1988. 9. Bracken, M. B., Shepard, M. J., Collins, W. F., Holford, T. R., Young, W., Baskin, D. S., Eisenberg, H. M., Flamm, E., Leo-Summers, 1., Maroon, J., Marshall, 1. F., Perot, P. 1., Peipmeier, J., Sonntag, V. K. H., Wagner, F. c.. Wilberger, J. E., and Winn, H. R.: A randomized, controlled trial of methylprednisolone or neloxone in the treatment of acute spinalcord injury. N. Engl. J. Med. 322:1405,1990. 10. Braughler, J. M., and Hall, E. D.: Current applications of "high-dose" steroid therapy for CNS injury. J. Neurosurg. 62:806, 1985. 11. Wolin, M. J., and Lavin, P. J. M.: Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am. J. Ophthalmol. 109:430, 1990.
Patients and Methods Traumatic optic neuropathy is defined as traumatic visual loss that occurs in the presence of an afferent pupillary defect without evidence of injury to the eye or optic nerve.Y Patients with such neuropathies were examined and treated at two trauma centers (Miami Valley Hospital, Dayton, Ohio and Kresge Eye Institute, Detroit Receiving Hospital, Detroit, Michigan). All patients received a complete neuroAccepted for publication Aug. 27, 1990. From the Kresge Eye Institute, Wayne State University, Detroit, Michigan (Drs. Spoor, Lensink, and Wilkinson); and Department of Ophthalmology, Wright State University School of Medicine, Dayton, Ohio (Dr. Hartel). Reprint requests to Thomas C. Spoor, M.D., F.A.C.S., Kresge Eye Institute, Wayne State University, 4717 St. Antoine, Detroit, MI 48201.
©AMERICAN JOURNAL OF OPHTHALMOLOGY
110:665-669,
ophthalmic examination and high-resolution computed tomography of the brain and orbits, including bone window images. Patients with associated concussive or penetrating ocular injuries were excluded from the study. Eight patients (Dayton) were treated with intravenous dexamethasone, 20.0 mg every six hours (approximately 0.25 mg Zkg of body weight for 48 hours). Thirteen patients (Detroit) were treated with intravenous methylprednisolone, 30.0 mg Zkg of body weight initially, followed two hours later by 15.0 mg/kg of body weight every six hours for 48 hours. In both groups, corticosteroids were tapered rapidly after 48 hours. The time between injury and initiation of treatment was variable, ranging from 8th hours to 15 days (mean, 4.2 days) in the group treated with intravenous methylprednisolone. Treatment with intravenous dexamethasone was initiated earlier (four hours to four days; mean, 17 hours). Seventeen patients were male and four patients were female. Motor vehicle accidents accounted for most of the injuries (ten), followed closely by assaults (eight) and falls (three). The assault group contained three patients with penetrating orbital injuries, two caused by knives and one caused by a BB pellet. These patients were included since eventual visual and motility recovery indicated that the apical orbital structures had not been transsected.
Results Thirteen patients were treated with intravenous megadoses of methylprednisolone (Tables 1 and 2), and eight patients were treated with high doses of intravenous dexamethasone (Tables 3 and 4). Patients treated with methylprednisolone received much higher doses of corticosteroids than those treated with dexamethasone (20 times the initial dose and ten DECEMBER,
1990
665
666
December, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
TABLE 1 CHARACTERISTICS OF PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY TREATED WITH MEGADOSE CORTICOSTEROIDS' CASE NO., SEX
INJURY TO
VISUAL ACUITY'
AGE (VRS), INITIAL
POSTPULSE
TRAUMA
TREATMENT FINAL
INTERVAL
FOLLOW-UP
CAUSE
INJURY
1,33, M NLP
NLP
NLP
2 days
3 weeks
Fall from truck
Optic canal
2,21, M 20/200
20/40
20/25
15 days
1 month
3,38, M HM 4.27, M 20/40 5.15, M 20/200
20/70 20/20 20/30
20/30 20/20 20/30
8 hours 7 days 8 days
2 weeks 6 weeks 6 months
Trimalar fracture. epidural hematoma Trirnalar fracture
6,31, M NLP
20/200
20/100
2'12 days
3 years
Motor vehicle accident Baseball bat Wrench to head Bike hit by train Knife to orbit
7,27, M NLP
NLP
20/50
2 days
1 week
8,25, M 20/200 9,40, M LP
20/20 20/400
20/20 20/25
24 hours 2 hours
10. 16, M HM
20/200
20/50
3 days
11,30. F
20/400
20/100
20/50
20 hours
12, 28. F
CF
20/400
20/30
12 hours
20/40
20/25
7 days
8 months Fist to face 2 112 months Motor vehicle accident 3 years BB to orbital apex 21/2 months Motor vehicle accident 3 weeks Gun shot wound to the orbit 2 months Fell and struck head
13,38, M 20/80
Knife up nose to orbit
Orbital roof and frontal fractures Pneumocephalus. orbital apex syndrome Orbital apex syndrome
COMMENT
Transcranial optic canal decompression, no improvement
Concomitant orbital apex syndrome resolved Transethmoidal canal decompression after corticosteroid failure
Orbital roof fracture
Transethmoidal decompression Facial fractures Orbital hemorrhage
Canthotomy, cantholysis before corticosteroids
Orbital roof fracture
'Patients treated with methylprednisolone, 30 mg/kg of body weight pulse. then 15 mg/kg of body weight every six hours. tNLP indicates no light perception; HM indicates hand motions; and CF indicates counting fingers,
times the subsequent doses). Most of the patients in both groups had marked improvement in visual function. No statistically significant difference was found between the two groups in final visual improvement (P = .3, chi-square test). Of eight patients treated with intravenous dexamethasone, seven of nine eyes had improved visual function. Of 13 patients treated with megadoses of intravenous methylprednisolone, 12 showed improved visual function. The interval between injury and initiation of treatment was variable. A long interval (mean, 4.2 days) between injury and treatment did not preclude improvement in visual function in most patients treated with megadose methylprednisolone. Few patients treated with highdose dexamethasone demonstrated dramatic visual recovery during treatment despite a
much shorter interval between injury and treatment (mean, 17 hours). Of 13 patients treated with megadose methylprednisolone, 11 had significantly improved visual function within 96 hours after the initiation of treatment. Only two of nine eyes in the group treated with dexamethasone demonstrated this rapid improvement in visual function. This difference was significant (P = .008). Three patients in the mega dose methylprednisolone group underwent subsequent surgical decompression of their optic canal by either a trans cranial (Case 1) or a transethmoidal route (Cases 7 and 10). The patient in Case 1 had an optic canal fracture on computed tomographic scans and an equivocal history of progressive visual loss to no light perception. Another patient (Case 10) had a BB pellet compressing the
Vol. 110, No.6
Traumatic Optic Neuropathy and Corticosteroids
TABLE 2 RESIDUAL VISUAL FIELD DEFECTS IN PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY'
CASE NO.
1 2 3 4 5
6 7
8
9
VISUAL ACUITY' INITIAL
NLP 20/200 HM 20/40
FINAL
NLP 20/25 20/30 20/20
VISUAL FIELD DEFECTS INITIAL
HM
11
20/400 20/50
12 13
CF 20/80
20/50
20/30 20/25
as lessening of central scotomas, sparing fixation, and increased peripheral field (Cases 5, 8, 11, and 13; Tables 2 and 4). Final visual fields, available on 15 eyes, demonstrated varying degrees of central and peripheral visual field loss (Tables 2 and 4).
FINAL
Discussion
Relative central scotoma 20/200 20/30 Superotemporal involving fixation NLP 20/100 NLP NLP 20/50 NLP 20/200 20/20 Inferonasal defect involving fixation LP 20/25 LP
10
667
Full
Superotemporal sparing fixation Inferior altitudinal Superior altitudinal Inferonasal defect sparing fixation Relative central scotoma. peripheral constriction Relative central HM scotoma, peripheral constriction Inferior altitudinal Relative central ininvolving fixation feronasal defect
Dense central sco- Relative central toma, peripheral scotoma, periphconstriction eral constriction
'Patients treated with methylprednisolone. 30 mg/kg of body weight pulse, then 15 mg/kg of body weight every six hours. tNLP indicates no light perception; LP indicates light perception; HM indicates hand motions; and CF indicates counting fingers.
optic nerve at the orbital apex and a medial optic canal fracture. Visual acuity improved from hand motions to 20/200 after intravenous methylprednisolone and subsequently improved to 20/50 after surgery. The visual acuity of one patient (Case 7) was no light perception after five days of intravenous methylprednisolone and improved to 20/50 after transethmoidal optic canal decompression." Initial visual acuity was worse than 20/200 in 20 eyes and totally blind with no light perception in eight eyes. Five of these eight eyes regained some visual function after treatment (Tables 2 and 4). Most patients were too critically injured or vision was too poor to obtain pretreatment visual fields. Visual fields were obtained before and after treatment in only five patients. Visual field improvement was defined
No consensus exists as to the appropriate treatment for patients with traumatic optic neuropathy. Lessell recently reported that only five of 25 untreated patients with indirect optic nerve injuries had improved visual function. Only one of four patients treated with low-dose corticosteroids had improved vision, whereas three of four patients treated with a combination of corticosteroids and trans ethmoidal optic canal decompression showed improvement in visual function. Of our 21 patients treated with intravenous corticosteroids, 17 had improved visual function. Many of our patients with improved visual acuity had residual visual field defects (Tables 2 and 4). When given within eight hours of injury, megadose corticosteroids have been shown to reduce paralysis and other disabilities but do not obviate neurologic deficits in patients with spinal cord injuries." The proposed mechanism is reduction of swelling in the injured tissue and prevention of cell degeneration. Large doses of methylprednisolone slow this degenerative process and increase the blood supply to the injured area, which decreases cell damage secondary to ischemia and hypoxemia." Possibly the corticosteroids decrease intraneural or extraneural edema and compression on the nerve fibers, increasing blood flow and salvaging some of the many nerve fibers subserving central visual acuity. This mechanism would explain the marked improvement in visual acuity and concomitant dense residual visual field defects found in some of our patients. Dosing schedules for high-dose corticosteroid therapy in the treatment of central nervous system trauma vary widely. Reported doses for dexamethasone range from 0.7 to 3.0 mg/kg of body weight, whereas methylprednisolone dosage schedules range from 0.6 to 30.0 mg Zkg of body weight. For the treatment of traumatic optic neuropathy, Anderson, Panje, and Gross" used dexamethasone in loading doses ranging from 16.0 to 60.0 mg followed by doses in the range of 20.0 mg every six hours.
668
December, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
TABLE 3 CHARACTERISTICS OF PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY TREATED WITH HIGH-DOSE CORTICOSTEROIDS' CASE NO., SEX
INJURY TO
VISUAL ACUITY'
AGE (VAS), INITIAL
POSTPULSE
TRAUMA
TREATMENT FINAL
INTERVAL
FOLLOW-UP
CAUSE
Motor vehicle accident Motor vehicle accident Motor vehicle accident Motor vehicle accident Motor vehicle accident Head pinned Hit with tool Motor vehicle accident Fell 2 stories
1,58, M
20/200
20/40
20/20
6 hours
11 months
2,17, M
NLP
NLP
20/30
5 hours
12 months
3,30, F
NLP
LP
20/300
6 hours
6 months
NLP
NLP
NLP
6 hours
6 months
4,18, M
NLP
NLP
NLP
5 hours
2 weeks
5,35, M 6,26, M 7,28, M
NLP LP HM
CF at 3 feet LP HM
20/25 HM CF at 4 feet
4 hours 4 days 7 hours
8 months 6 weeks 5 weeks
8.19, M
20/800
20/25
20/25
9 hours
2 months
INJURY
LeFort III fracture Closed head injury, pneumocephalus
Multiple orbital fracture
Skull fracture Orbit floor and maxilla fracture
'Patients treated with dexamethasone, 20 mg/kg of body weight every six hours. tNLP indicates no light perception; HM indicates hand motions; and CF indicates counting fingers.
Our rationale for using mega dose methylprednisolone to treat traumatic optic neuropathy is based largely on the work done by Braughler and Hall." They maintained that massive doses of corticosteroids (dexamethasone, 6,0 mg/kg of body weight, and methylprednisolone, 30.0 mg/kg of body weight) exhibit a different pharmacologic effect than the standard dose's glucocorticosteroid effect, They cited several examples of both experimental and clinical evidence demonstrating a sharp dose-response curve for methylprednisolone in massive-dose ranges. They believe, based on pharmacokinetics, that methylprednisolone, 30,0 mg zkg of body weight, should be given as soon as possible after injury, followed two hours later and every six hours after that by a dose of 15.0 mg Zkg of body weight. Our patients treated with the megadose methylprednisolone regimen improved much more quickly than those treated with high-dose dexamethasone (P = .008). However, initial visual acuity was not comparable, with a predominance of totally blind eyes (three eyes with light perception) in the dexamethasone group. Final visual results were not significantly different between the two groups (P = .3). Treatment with intravenous corticosteroids seemed to im-
prove visual prognosis whether administered in high doses or megadoses. Two of six totally blind untreated eyes in the TABLE 4 RESIDUAL VISUAL FIELD DEFECTS IN PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY'
CASE NO.
VISUAL FIELD DEFECTS
VISUAL ACUITY' INITIAL
FINAL
1 20/200 20/20 2 NLP 20/30 3 NLP 20/300 NLP NLP 4 NLP NLP 5 NLP 20/25 HM 6 LP CF at 4 feet 7 HM 8 20/800 20/25
INITIAL
FINAL
NLP NLP NLP NLP NLP
Peripheral constriction Temporal and peripheral loss Nasal peripheral loss Relative central scotoma NLP Inferonasal residual island of vision only
Nasal peripheral loss
'Patients treated with dexamethasone. 20 mg/kg of body weight every six hours. tNLP indicates no light perception; LP indicates light perception; HM indicates hand motions; and CF indicates counting fingers.
Vol. 110, No.6
Traumatic Optic Neuropathy and Corticosteroids
series described by Lessell? regained visual acuity of counting fingers and 10/200. Wolin and Lavin" described four patients who recovered vision after total blindness. Three of these patients were treated with corticosteroids, and visual acuity in one patient improved spontaneously. We agree with Wolin and Lavin!' in questioning the role of surgical decompression of the optic canal in patients with sudden, total visual loss. Of our patients, seven (eight eyes) had an initial visual acuity of no light perception after injury. Five of these eyes regained significant visual function after corticosteroid therapy. Visual acuity in two patients improved to better than 20/20 and 20/25, and visual acuity in two other patients improved to 20/ 100 and 20/300. An additional patient did not respond to megadose corticosteroids but did respond to transethmoidal optic canal decempression." Visual acuity in three other eyes remained no light perception despite high-dose dexamethasone (Cases 2 and 3, Table 3) and megadose methylprednisolone followed by transcranial optic canal decompression (Case 1, Table 1). Sudden total blindness does not preclude recovery of visual function and should not rule out corticosteroid treatment. Although most patients had indirect injury to the optic nerves related to facial fractures, some patients received direct, apparently penetrating optic nerve injuries that resulted in total blindness (Cases 6 and 7, Table 1). One patient recovered useful vision after treatment with mega dose corticosteroids. The other patient did not respond to megadose corticosteroids but did recover useful vision after trans ethmoidal optic canal decompression. We cannot predict which injured optic nerves will improve with corticosteroid treatment. We believe that a short course of high-dose or megadose corticosteroids may be useful for patients with traumatic optic neuropathy. The mechanism of injury should not preclude a response to corticosteroid therapy unless obvious avulsion or transsection of the optic nerve is apparent on examination or on computed tomographic scans. Our data are uncontrolled
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but suggest that high doses of intravenous corticosteroids may help restore vision in patients with traumatic optic neuropathy.
References 1. Hughes, B.: Indirect injury to the optic nerves and chiasm. Bull. Johns Hopkins Hosp. 111:98, 1962. 2. Anderson, R. 1., Panje, W. R., and Gross, C. E.: Optic nerve blindness following blunt forehead trauma. Ophthalmology 89:445, 1982. 3. Matsuzaki, H., Kitahara, K., Kawai, K., and Kumita, M.: The nonsurgical treatment for damage to the intracanalicular portion of the optic nerve. In Highlights in Neuro-Ophthalmology. Proceedings of the International Neuro-Ophthalmology Society, Hakone, Japan. Amsterdam, Aeolus Press, 1987, pp. 27-35. 4. Fukado, Y.: Results in 400 cases of surgical decompression of the optic nerve. Mod. Prob. Ophthalmol. 14:478, 1975. 5. Fugitani, T., Inoue, K., and Takahashi, T.: Indirect traumatic optic neuropathy. Visual outcome of operative and non operative cases. Ipn. J. Ophthalmol. 30:125, 1986. 6. Walsh, F. B., and Hoyt, W. F.: Clinical NeuroOphthalmology, vol. 3, ed. 3. Baltimore, Williams and Wilkins, 1969, p. 2376. 7. Lessell, S.: Indirect optic nerve trauma. Arch. Ophthalmol. 107:382, 1989. 8. Spoor, T. C., and Mathog, R.: Restoration of vision after optic canal decompression following five days of total blindness and mega dose corticosteroid therapy. Arch. Ophthalmol. 104:804, 1988. 9. Bracken, M. B., Shepard, M. J., Collins, W. F., Holford, T. R., Young, W., Baskin, D. S., Eisenberg, H. M., Flamm, E., Leo-Summers, 1., Maroon, J., Marshall, 1. F., Perot, P. 1., Peipmeier, J., Sonntag, V. K. H., Wagner, F. c.. Wilberger, J. E., and Winn, H. R.: A randomized, controlled trial of methylprednisolone or neloxone in the treatment of acute spinalcord injury. N. Engl. J. Med. 322:1405,1990. 10. Braughler, J. M., and Hall, E. D.: Current applications of "high-dose" steroid therapy for CNS injury. J. Neurosurg. 62:806, 1985. 11. Wolin, M. J., and Lavin, P. J. M.: Spontaneous visual recovery from traumatic optic neuropathy after blunt head injury. Am. J. Ophthalmol. 109:430, 1990.
