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Spontaneous Visual Recovery From Traumatic Optic Neuropathy After Blunt Head Injury
Spontaneous Visual Recovery From Traumatic Optic Neuropathy After Blunt Head Injury Mitchell
J.
Wolin, M.D., and Patrick
Four patients who developed immediate blindness (no light perception) after indirect traumatic optic neuropathy caused by blunt head injury recovered vision without surgical intervention. In one patient, whose affected eye recovered to a visual acuity of 20/50 + 2, corticosteroids were not used. In two of the other patients, visual recovery began before corticosteroids were instituted. One patient recovered a visual acuity of R.E.: 20/15, one recovered a visual acuity of L.E.: 20/25 - 2, and one recovered a visual acuity of R.E.: 20/200 but with useful temporal field vision. Many investigators advocate aggressive surgical therapy for indirect neuropathy, particularly when corticosteroids fail. Significant recovery may occur despite no light perception, however, with medical therapy or even without therapy. BLUNT HEAD TRAUMA, particularly to the forehead, may cause loss of vision as a result of optic nerve injury, even when the degree of trauma seems trivial.!" The optic nerve is most vulnerable in, or at either end of, the bony optic canal, and at the muscle cone.' Direct injury may result from a fracture through the bony canal that severs or compresses the nerve, or bone fragments that lacerate the nerve." The exact mechanism by which indirect injury to the nerve occurs remains uncertain. Shearing forces caused by abrupt deceleration of the skull may damage optic nerve fibers, but ischemia, caused by injury to small nutrient vessels, is the more likely mechanism.Pr-"
Accepted for publication Jan. 29, 1990. From the Departments of Ophthalmology (Drs. Wolin and Lavin) and Neurology (Dr. Lavin), Vanderbilt University Medical Center, Nashville, Tennessee. Reprint requests to Patrick J. M. Lavin, M.D., 2100 Pierce Ave., Room 351, Nashville, TN 37212.
430
J.
M. Lavin, M.D.
Immediate loss of vision (no light perception) on impact indicates a severe optic nerve injury with a poor prognosis for recovery; a short period of vision (lucid interval) before deterioration suggests a potentially reversible process 7,8 and may warrant surgical intervention. The course of indirect optic nerve injury is unpredictable, making it difficult to define the roles of both corticosteroids in high doses and urgent optic nerve decornpression.v" Our four patients sustained optic nerve blindness (no light perception) caused by blunt head injury, but all recovered useful vision.
Case Reports Case 1 A 25-year-old man sustained a head injury in a motor vehicle accident. It was not clear whether he had lost consciousness; he was alert on arrival at the emergency room but could not remember details of the accident. He had a left zygomatic fracture under a large, raised skin and muscle flap. His visual acuity was R.E.: 20/25 and L.E.: no light perception. The right pupil was 3 mrn, and the left pupil was 7 mm. The right pupil reacted briskly to light. The left pupil was amaurotic, with an intact consensual response. Ocular motility was normal. A small hyphema was present in the left eye. Intraocular pressures were R.E.: 25 mm Hg and L.E.: 33 mm Hg, by Schietz tonometry. Berlin's edema was observed superiorly in the left eye. Orbital computed tomography showed a soft tissue density consistent with hemorrhage behind the left globe (Fig. 1). Comminuted fractures were present at the apex of the orbit near the optic canal, but neither impingement of the optic nerve nor fracture through the canal were seen (Fig. 1). Over the next six days, the patient's visual acuity remained L.E.: no light perception. Timolol maleate (0.5%) was administered for
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Fig. 1 (Wolin and Lavin). Patient 1. Left, Computed tomographic scan shows a soft tissue density just posterior to the left globe (Patient 1). Right, Comminuted fracture of the posterior cone of the orbit without optic nerve impingement, and multiple fractures of the medial orbital wall on the left with opacification of the ethmoid air cells are shown.
the first five days with normalization of ocular tension. No further hemorrhage occurred in the anterior chamber. Three weeks after the injury, the patient's visual acuity was R.E.: 20/30 and L.E.: 20/50, and the left pupil reacted partially to direct light. By six weeks, visual acuity in the left eye had improved to 20/40 - 2, although a relative afferent pupillary defect was still present. His left visual field showed mild, generalized constriction without segmental or focal deficits (Fig. 2). Five months later, the patient had left optic atrophy, but his visual acuity was R.E.: 20/30 + 3 and L.E.: 20/50 + 2 without correction. Case 2 A 16-year-old boy was injured in a motor vehicle accident when he, restrained by a lap belt without a shoulder harness, struck his face
on the windshield. He said he had not lost consciousness. In the emergency room, indirect ophthalmoscopy disclosed no light perception in both eyes. The patient's pupils were 4 mm in both eyes with a trace reaction to direct light in the right eye but none in the left eye. He had a partial-thickness right corneal laceration. Intraocular pressure was 30 mm Hg in the right eye and 15 mm Hg in the left eye by digital pneumotonometry. Ophthalmoscopy disclosed a peripapillary flame-shaped hemorrhage just temporal to the disk and mild Berlin's edema in the right eye. He had a 30% hyphema in the left eye; no lacerations were seen. Repeat examination three days later showed some mild vitreous hemorrhage in the left eye. Choroidal rupture was suspected superiorly. Orbital computed tomography showed distortion of the left globe. There were bone fragments in both orbital
Fig. 2 (Wolin and Lavin). Patient 1. Goldmann visual field examina-
tion performed 11 weeks after injury shows mild constriction with reduction in central sensitivity of the field of left eye.
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Fig. 3 (Wolin and Lavin). Patient 2. Computed tomographic scan shows multiple comminuted fractures of the nasal and ethmoid bones, the lateral wall of the left orbit, bone fragments in the soft tissues near the right globe, and fluid in the nasal sinuses.
apices, but no definite nerve compression was identified (Fig. 3). The sclera appeared intact. Subsequent ultrasound disclosed no evidence of globe rupture or laceration. Because the patient still had no light perception in either eye the day after injury, intravenous dexamethasone (10 mg every six hours) was administered. A few hours later, the patient's visual acuity was found to be R.E.: counting fingers and L.E.: hand motions. On the following day, his visual acuity was R.E.: 20/300 and L.E.: counting fingers, and five weeks later it was R.E.: 20/30 and L.E.: 20/200. The vitreous hemorrhage in the left eye cleared gradually. Later ophthalmoscopic examination confirmed areas of choroidal rupture superiorly in the left eye, without evidence of scleral rupture. Six months later, the patient's visual acuity was R.E.: 20/25 and L.E.: 20/50 - 2. The left pupil was still unreactive. Because of a traction retinal detachment in the left eye, he had a vitrectomy membrane peel and cryotherapy. The patient's visual acuity 18 months after the accident was R.E.: 20/15 and L.E.: 20/25 + 2 with relatively normal confrontation visual fields, but mild left optic atrophy. Case 3 A 17-year-old boy was injured in a motor vehicle accident when he, unrestrained by a seatbelt, struck his face on the dashboard. He did not lose consciousness. On arrival at the emergency room, he had no light perception in either eye, and his pupils were fixed and dilat-
April, 1990
Fig. 4 (Wolin and Lavin). Patient 3. Computed tomographic scan shows multiple nasal and ethmoid fractures.
ed. He had periorbital and nasal swelling with multiple facial lacerations. His fundi were not visualized. He was transferred to a secondary facility where on arrival his visual acuity was R.E.: no light perception and L.E.: light perception without projection. A computed tomographic scan showed fractures of the nose, orbital floors, walls of the ethmoid sinuses, cribriform plates, and periorbital rims. The right optic nerve appeared severed (Fig. 4). The following procedures were done: internal fixation of the nasal fractures, closed reduction of the nasal septum fracture, a left orbital floor implant with removal of a small piece of bone from the posterior orbit, and debridement and closure of the facial fractures. The optic nerve canal was not decompressed. After surgery, the patient continued to have a visual acuity of R.E.: no light perception and L.E.: bare light perception. Because of persistent light perception, he was transferred to a tertiary facility three days after the injury for consideration for optic canal decompression. On arrival, his visual acuity was R.E.: no light perception and L.E.: light perception. Both pupils were fixed and dilated, and he had complete bilateral ophthalmoplegia. His eyes were swollen shut with periorbital ecchymoses and lacerations as well as chemosis bilaterally. He also had a right subconjunctival hemorrhage. No blood was seen in either anterior chamber. An adequate view of the right fundus was not obtained because of the periorbital swelling. Examination of the left fundus disclosed choroidal rupture inferior to the optic disk. Intravenous dexamethasone, 10 mg initially and 4 mg every six hours thereafter, was administered. Later that
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Fig. 5 (Wolin and Lavin). Patient 3. Goldmann visual field examination performed ten weeks after surgery shows a blind right eye and partial recovery of the field of the left eye.
evening, the patient's visual acuity was R.E.: no light perception and L.E.: counting fingers at three feet. On the fourth day after initiation of corticosteroids, his visual acuity was R.E.: no light perception and L.E.: 20/400. He was discharged on the sixth day on a regimen of tapering dexamethasone; his visual acuity was R.E.: no light perception and L.E.: 20/400. Ten weeks later, the patient's visual acuity was R.E.: no light perception and L.E.: 20/25 2 without correction. He had a right relative afferent pupillary defect. His left visual field showed a large superior temporal defect with a relative central scotoma (Fig. 5). He could read only two of 24 Ishihara color plates and scored 60 points on Sahlgren's saturation test (normal, < 15). Ophthalmoscopy showed a glial scar obscuring the view of the right optic disk; the left disk was partially atrophic. Case 4 A 23-year-old man, unrestrained by a seatbelt, was asleep in the passenger seat of a truck when it ran off the road and overturned. He was thrown from the truck and sustained a blunt head injury with a brief loss of consciousness. In the emergency room, he was alert and oriented and complained that he was unable to perceive light with his right eye at the scene of the accident and on arriving at the emergency room. Within 30 minutes of his arrival at the emergency room, an ophthalmologist found his visual acuity to be R.E.: counting fingers at two feet and L.E.: 20/20. His right pupil was dilated; he had both a right afferent and efferent pupillary defect. He had ecchymosis of the right upper eyelid with periorbital swelling. Results of direct and indirect ophthalmoscopy were normal. He had complete loss of abduction and some impairment of elevation and depression
of the right eye; the left eye was normal. He had depression of the malar emminence on the right. Tactile ocular tensions were normal. He also had a puncture wound in the mid forehead associated with fractures of the anterior and posterior tables of the frontal sinus and laceration of the dura mater. A computed tomographic scan of the head showed free air in the anterior cranial fossa on the right, fractures through the anterior walls of the maxillary sinuses with air in the orbit, air fluid levels in the ethmoid and maxillary sinuses on the right, and a fracture through the right optic foramen. There was no evidence of bony impingement of the right optic nerve (with coronal views), but the superior orbital fissure appeared distorted. The following day, a regimen of 8 mg of intravenous dexamethasone was instituted every eight hours. Nine days later, the patient underwent an obliteration and cranialization procedure, with an osteoplastic frontal sinus flap. Six weeks later, the patient's visual acuity, without correction, was R.E.: 2/200 and L.E.: 20/20. Color vision was impaired in the right eye (he could read none of the Ishihara color plates), but was normal in the left eye. Formal visual fields on a Goldmann perimeter showed a large central scotoma with a peripheral rim of preserved vision temporally and inferiorly (Fig. 6). He had a relative afferent pupillary defect and marked optic atrophy in the right eye.
Discussion
In these four patients, indirect injury to the optic nerve was the predominant cause of visu-
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Fig. 6 (Wolin and Lavin). Patient 4. Goldmann visual field examination performed six weeks after surgery shows partial recovery of the field of the right eye.
alloss. The first patient had no light perception in the left eye with an amaurotic dilated pupil that reacted consensually. The degree of hypherna and retinal edema did not account for the severity of visual loss. The second patient had no light perception in either eye, and his intraocular injuries were not sufficient to account for complete loss of vision. The third patient had no light perception in either eye when examined in the emergency room, but a few hours later, he had bare light perception in the left eye. Vision in the left eye began to recover before corticosteroids were introduced, and the further improvement might have been spontaneous. The surgical procedure involved reduction of nasal fractures, repair of the left orbital floor, and removal of an orbital bone spicule remote from the orbital apex; the optic nerve was not decompressed. The fourth patient also had some improvement in vision before the administration of corticosteroids. These patients are remarkable for the extent of recovery after the condition of no light perception. The first patient is also remarkable for the long interval between the head injury and recovery of vision, particularly in the absence of corticosteroid therapy. The optic nerve dysfunction in our patients may have been caused by transient failure of conduction (neuropraxia), edema, or transient ischemia of the optic nerve. In 1982, Anderson, Panje, and Cross" advocated the use of high-dose corticosteroids in traumatic optic neuropathy based on their experience with seven patients. Two patients recovered significant vision coincident with the use of corticosteroids, and two patients had a lesser degree of recovery, one after decompression of a subperiosteal orbital hematoma. Since then, there have been reports of similar suecesses,3,9-11 although Tang and associates," in a series of 37 patients, found corticosteroids un-
successful. Several recent studies have reported the lack of efficacy, indeed sometimes harmful effects, of corticosteroids in other neurologic disorders, including cerebral trauma." ischemic stroke," intracerebral hemorrhage," spinal cord injury.J'':" and acute polyneuropathy." The first patient recovered useful vision (from no light perception) with neither corticosteroids nor surgical intervention. The third and fourth patients began to recover vision before the initiation of corticosteroids. The second patient had some improvement soon after the introduction of corticosteroids, but had a prolonged interval between the injury and significant recovery of vision. Our patients received neither megadose corticosteroids nor hyperosmolar agents. A spontaneous recovery is frequently attributed to the introduction of therapy. Only a controlled randomized trial, or observations of definite deterioration on withdrawal of medication with subsequent recovery on re-introduction in a number of patients, will clarify the efficacy of corticosteroids. Such a controlled randomized trial, however, is probably not feasible." A number of reports 2,6,9,20,21 of successful decompression of traumatic optic neuropathy after optic nerve injury support the role of surgery, even when it is delayed as long as five days II; Spoor and Mathog describe such a patient who had a penetrating knife wound." Had our patients undergone decompressive surgery, the results would have been considered successful. When a compressive hematoma is present, the role of surgery seems clear; however, in the absence of such a hematoma, even with depressed bone fragments, the indications for surgery are less obvious. Whether a craniotomy with decompression of the optic nerve canal and falciform ligament is superior to the transethmoidal approach is also controversial." Re-
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ports of optic nerve decompression are difficult to evaluate because they are uncontrolled and not randomized. 2,6,8,9.2o.24 In the series of Fukado" and Niho, Niho, and Niho,23 the operative results were excellent; these studies, however, are criticizedv" for poor documentation and patient selection. Investigators, however, have found little benefit in optic nerve decompression in patients who have had immediate blindness caused by injury.2.12.24 Although a controlled randomized trial is probably not feasible, a central data bank for the accumulation and analysis of information on patients with indirect optic nerve injury may help clarify the management of this condition." The results of this study illustrate the potential for spontaneous recovery in patients with immediate blindness after injury and contradict the idea that an amaurotic pupil indicates irreversible visual loss." We believe that the only clear indication for surgical intervention in indirect optic nerve trauma, in the absence of a compressive lesion, is where visual loss initially improves with corticosteroid therapy and then repeatedly deteriorates with tapered doses.
References 1. Turner, J. W. A.: Indirect injuries of the optic nerve. Brain 66:140, 1943. 2. Anderson, B. L., Panje, W. R., and Gross, C. E.: Optic nerve blindness following blunt forehead trauma. Ophthalmology 89:445, 1982. 3. Brooks, A. M., and Cairns, J. D.: Contusion injuries of the optic nerve. Aust. N.Z. J. Ophthalmol. 14:269,1986. 4. Crompton, M. R.: Visual lesions in closed head injury. Brain 93:785, 1970. 5. Edmund, J., and Godtfredsen, E.: Unilateral optic atrophy following head injury. Acta Ophthalmol. 41:693, 1963. 6. Lipkin, A. F., Woodson, G. E., and Miller, R. D.: Visual loss due to orbital fracture. The role of early reduction. Arch. Otolaryngol. Head Neck Surg. 113:81,1987. 7. Kennerdell, J. 5., Amsbaugh, C. A., and Myers, E. N.: Transantral-ethmoidal decompression of optic canal fracture. Arch. Ophthalmol. 94:1040, 1976. 8. Kline, L. B., Morawetz, R. B., and Swaid, N. 5.: Indirect injury of the optic nerve. Neurosurgery 14:756,1984. 9. Noble, M. J., and McFadzean, R.: Indirect injury to the optic nerves and chiasm. Neuro-Ophthalmology 7:341, 1987. 10. Katz, B., Herschler, J., and Brick, D. c.: Orbital
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hemorrhage and prolonged blindness. Treatable posterior optic neuropathy. Br. J. Ophthalmol. 67:549, 1983. 11. Spoor, T. c., and Mathog, R. H.: Restoration of vision after optic canal decompression. Arch. Ophthalmol. 104:804, 1986. 12. Tang, R. A., u. H. K., Regner, V., Bridges, M. B., and Prager, T. c.: Traumatic optic neuropathy. Analysis of 37 cases. ARVO abstracts. Supplement to Invest. Ophthalmol. Vis. Sci. Philadelphia, J. B. Lippincott, 1986, p. 102. 13. Dearden, N. M., Gibson, J.S., McDowall, D. G., Gibson, R. M., and Cameron, M. M.: Effects of high-dose dexamethasone on outcome from severe head injury. J. Neurosurg. 64:81, 1986. 14. Norris, J. W., and Hachinski, V. c.. Megadose steroid therapy in ischemic stroke. Stroke 16:150, 1985. 15. Poungvarin, N., Bhoopat, W., Viriyavejakul, A., Rodprasert, P., Buranasiri, P., Sukondhabhant, 5., Hensley, M. J., and Strom, B. L.: Effects of dexamethasone in primary supratentorial intracerebral hemorrhage. N. Engl. J. Med. 316:1229, 1987. 16. White, R. J.: Advances in the treatment of cervical cord injuries. Clin. Neurosurg. 26:556, 1979. 17. Bracken, M. B., Shepard, M. J., Hellenbrand, K. G., Collins, W. F., Leo, L. 5., Freeman, D. F., Wagner, F. c.. Flamm, E. 5., Eisenberg, H. M., Goodman, J. H., Perot, P.1., Green, B. A., Grossman, R. G., Meagher, J. N., Young, W., Fischer, B., Clifton, G. L., Hunt, W. E., and Rifkinson, N.: Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the national acute spinal cord injury study. J. Neurosurg. 63:704, 1985. 18. Hughes, R. A. c.. Newsom-Davis, J. M., Perkins, G. D., and Peirce, J. M.: Controlled trial of prednisolone in acute polyneuropathy. Lancet 2:750, 1978. 19. Lessell, 5.: Indirect optic nerve trauma. Arch. Ophthalmol. 107:382, 1989. 20. Waga, 5., Kubo, Y., Sakakura, M.: Transfrontal intradural microsurgical decompression for traumatic optic nerve injury. Acta Neurochir. (Wien) 91:42, 1988. 21. Goldware, 5., Sylvester, R., and Baker, L.: Delayed post traumatic optic neuropathy with recovery after unroofing of optic canal. Neuro-Ophthalmology 1:77, 1980. 22. Fukado, Y.: Results in 400 cases of surgical decompression of the optic nerve. Mod. Probl. Ophthalmol. 14:474, 1975. 23. Niho, 5., Niho, M., and Niho, K.: Decompression of 16 optic canals by the transethmoidal route. Can. J. Ophthalmol. 5:22, 1970. 24. Hughs, B.: Indirect injury of the optic nerves and chiasm. Bull. Johns Hopkins Hosp. 111:98, 1962. 25. Walsh, F. B.: Trauma involving the anterior visual pathways. In Freeman, H. M. (ed.): Ocular Trauma. New York, Appleton-Century-Crofts, 1979, ch. 35, pp. 335-351.
J.
Wolin, M.D., and Patrick
Four patients who developed immediate blindness (no light perception) after indirect traumatic optic neuropathy caused by blunt head injury recovered vision without surgical intervention. In one patient, whose affected eye recovered to a visual acuity of 20/50 + 2, corticosteroids were not used. In two of the other patients, visual recovery began before corticosteroids were instituted. One patient recovered a visual acuity of R.E.: 20/15, one recovered a visual acuity of L.E.: 20/25 - 2, and one recovered a visual acuity of R.E.: 20/200 but with useful temporal field vision. Many investigators advocate aggressive surgical therapy for indirect neuropathy, particularly when corticosteroids fail. Significant recovery may occur despite no light perception, however, with medical therapy or even without therapy. BLUNT HEAD TRAUMA, particularly to the forehead, may cause loss of vision as a result of optic nerve injury, even when the degree of trauma seems trivial.!" The optic nerve is most vulnerable in, or at either end of, the bony optic canal, and at the muscle cone.' Direct injury may result from a fracture through the bony canal that severs or compresses the nerve, or bone fragments that lacerate the nerve." The exact mechanism by which indirect injury to the nerve occurs remains uncertain. Shearing forces caused by abrupt deceleration of the skull may damage optic nerve fibers, but ischemia, caused by injury to small nutrient vessels, is the more likely mechanism.Pr-"
Accepted for publication Jan. 29, 1990. From the Departments of Ophthalmology (Drs. Wolin and Lavin) and Neurology (Dr. Lavin), Vanderbilt University Medical Center, Nashville, Tennessee. Reprint requests to Patrick J. M. Lavin, M.D., 2100 Pierce Ave., Room 351, Nashville, TN 37212.
430
J.
M. Lavin, M.D.
Immediate loss of vision (no light perception) on impact indicates a severe optic nerve injury with a poor prognosis for recovery; a short period of vision (lucid interval) before deterioration suggests a potentially reversible process 7,8 and may warrant surgical intervention. The course of indirect optic nerve injury is unpredictable, making it difficult to define the roles of both corticosteroids in high doses and urgent optic nerve decornpression.v" Our four patients sustained optic nerve blindness (no light perception) caused by blunt head injury, but all recovered useful vision.
Case Reports Case 1 A 25-year-old man sustained a head injury in a motor vehicle accident. It was not clear whether he had lost consciousness; he was alert on arrival at the emergency room but could not remember details of the accident. He had a left zygomatic fracture under a large, raised skin and muscle flap. His visual acuity was R.E.: 20/25 and L.E.: no light perception. The right pupil was 3 mrn, and the left pupil was 7 mm. The right pupil reacted briskly to light. The left pupil was amaurotic, with an intact consensual response. Ocular motility was normal. A small hyphema was present in the left eye. Intraocular pressures were R.E.: 25 mm Hg and L.E.: 33 mm Hg, by Schietz tonometry. Berlin's edema was observed superiorly in the left eye. Orbital computed tomography showed a soft tissue density consistent with hemorrhage behind the left globe (Fig. 1). Comminuted fractures were present at the apex of the orbit near the optic canal, but neither impingement of the optic nerve nor fracture through the canal were seen (Fig. 1). Over the next six days, the patient's visual acuity remained L.E.: no light perception. Timolol maleate (0.5%) was administered for
©AMERICAN JOURNAL OF OPHTHALMOLOGY
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APRIL,
1990
Vol. 109, No.4
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Fig. 1 (Wolin and Lavin). Patient 1. Left, Computed tomographic scan shows a soft tissue density just posterior to the left globe (Patient 1). Right, Comminuted fracture of the posterior cone of the orbit without optic nerve impingement, and multiple fractures of the medial orbital wall on the left with opacification of the ethmoid air cells are shown.
the first five days with normalization of ocular tension. No further hemorrhage occurred in the anterior chamber. Three weeks after the injury, the patient's visual acuity was R.E.: 20/30 and L.E.: 20/50, and the left pupil reacted partially to direct light. By six weeks, visual acuity in the left eye had improved to 20/40 - 2, although a relative afferent pupillary defect was still present. His left visual field showed mild, generalized constriction without segmental or focal deficits (Fig. 2). Five months later, the patient had left optic atrophy, but his visual acuity was R.E.: 20/30 + 3 and L.E.: 20/50 + 2 without correction. Case 2 A 16-year-old boy was injured in a motor vehicle accident when he, restrained by a lap belt without a shoulder harness, struck his face
on the windshield. He said he had not lost consciousness. In the emergency room, indirect ophthalmoscopy disclosed no light perception in both eyes. The patient's pupils were 4 mm in both eyes with a trace reaction to direct light in the right eye but none in the left eye. He had a partial-thickness right corneal laceration. Intraocular pressure was 30 mm Hg in the right eye and 15 mm Hg in the left eye by digital pneumotonometry. Ophthalmoscopy disclosed a peripapillary flame-shaped hemorrhage just temporal to the disk and mild Berlin's edema in the right eye. He had a 30% hyphema in the left eye; no lacerations were seen. Repeat examination three days later showed some mild vitreous hemorrhage in the left eye. Choroidal rupture was suspected superiorly. Orbital computed tomography showed distortion of the left globe. There were bone fragments in both orbital
Fig. 2 (Wolin and Lavin). Patient 1. Goldmann visual field examina-
tion performed 11 weeks after injury shows mild constriction with reduction in central sensitivity of the field of left eye.
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Fig. 3 (Wolin and Lavin). Patient 2. Computed tomographic scan shows multiple comminuted fractures of the nasal and ethmoid bones, the lateral wall of the left orbit, bone fragments in the soft tissues near the right globe, and fluid in the nasal sinuses.
apices, but no definite nerve compression was identified (Fig. 3). The sclera appeared intact. Subsequent ultrasound disclosed no evidence of globe rupture or laceration. Because the patient still had no light perception in either eye the day after injury, intravenous dexamethasone (10 mg every six hours) was administered. A few hours later, the patient's visual acuity was found to be R.E.: counting fingers and L.E.: hand motions. On the following day, his visual acuity was R.E.: 20/300 and L.E.: counting fingers, and five weeks later it was R.E.: 20/30 and L.E.: 20/200. The vitreous hemorrhage in the left eye cleared gradually. Later ophthalmoscopic examination confirmed areas of choroidal rupture superiorly in the left eye, without evidence of scleral rupture. Six months later, the patient's visual acuity was R.E.: 20/25 and L.E.: 20/50 - 2. The left pupil was still unreactive. Because of a traction retinal detachment in the left eye, he had a vitrectomy membrane peel and cryotherapy. The patient's visual acuity 18 months after the accident was R.E.: 20/15 and L.E.: 20/25 + 2 with relatively normal confrontation visual fields, but mild left optic atrophy. Case 3 A 17-year-old boy was injured in a motor vehicle accident when he, unrestrained by a seatbelt, struck his face on the dashboard. He did not lose consciousness. On arrival at the emergency room, he had no light perception in either eye, and his pupils were fixed and dilat-
April, 1990
Fig. 4 (Wolin and Lavin). Patient 3. Computed tomographic scan shows multiple nasal and ethmoid fractures.
ed. He had periorbital and nasal swelling with multiple facial lacerations. His fundi were not visualized. He was transferred to a secondary facility where on arrival his visual acuity was R.E.: no light perception and L.E.: light perception without projection. A computed tomographic scan showed fractures of the nose, orbital floors, walls of the ethmoid sinuses, cribriform plates, and periorbital rims. The right optic nerve appeared severed (Fig. 4). The following procedures were done: internal fixation of the nasal fractures, closed reduction of the nasal septum fracture, a left orbital floor implant with removal of a small piece of bone from the posterior orbit, and debridement and closure of the facial fractures. The optic nerve canal was not decompressed. After surgery, the patient continued to have a visual acuity of R.E.: no light perception and L.E.: bare light perception. Because of persistent light perception, he was transferred to a tertiary facility three days after the injury for consideration for optic canal decompression. On arrival, his visual acuity was R.E.: no light perception and L.E.: light perception. Both pupils were fixed and dilated, and he had complete bilateral ophthalmoplegia. His eyes were swollen shut with periorbital ecchymoses and lacerations as well as chemosis bilaterally. He also had a right subconjunctival hemorrhage. No blood was seen in either anterior chamber. An adequate view of the right fundus was not obtained because of the periorbital swelling. Examination of the left fundus disclosed choroidal rupture inferior to the optic disk. Intravenous dexamethasone, 10 mg initially and 4 mg every six hours thereafter, was administered. Later that
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Fig. 5 (Wolin and Lavin). Patient 3. Goldmann visual field examination performed ten weeks after surgery shows a blind right eye and partial recovery of the field of the left eye.
evening, the patient's visual acuity was R.E.: no light perception and L.E.: counting fingers at three feet. On the fourth day after initiation of corticosteroids, his visual acuity was R.E.: no light perception and L.E.: 20/400. He was discharged on the sixth day on a regimen of tapering dexamethasone; his visual acuity was R.E.: no light perception and L.E.: 20/400. Ten weeks later, the patient's visual acuity was R.E.: no light perception and L.E.: 20/25 2 without correction. He had a right relative afferent pupillary defect. His left visual field showed a large superior temporal defect with a relative central scotoma (Fig. 5). He could read only two of 24 Ishihara color plates and scored 60 points on Sahlgren's saturation test (normal, < 15). Ophthalmoscopy showed a glial scar obscuring the view of the right optic disk; the left disk was partially atrophic. Case 4 A 23-year-old man, unrestrained by a seatbelt, was asleep in the passenger seat of a truck when it ran off the road and overturned. He was thrown from the truck and sustained a blunt head injury with a brief loss of consciousness. In the emergency room, he was alert and oriented and complained that he was unable to perceive light with his right eye at the scene of the accident and on arriving at the emergency room. Within 30 minutes of his arrival at the emergency room, an ophthalmologist found his visual acuity to be R.E.: counting fingers at two feet and L.E.: 20/20. His right pupil was dilated; he had both a right afferent and efferent pupillary defect. He had ecchymosis of the right upper eyelid with periorbital swelling. Results of direct and indirect ophthalmoscopy were normal. He had complete loss of abduction and some impairment of elevation and depression
of the right eye; the left eye was normal. He had depression of the malar emminence on the right. Tactile ocular tensions were normal. He also had a puncture wound in the mid forehead associated with fractures of the anterior and posterior tables of the frontal sinus and laceration of the dura mater. A computed tomographic scan of the head showed free air in the anterior cranial fossa on the right, fractures through the anterior walls of the maxillary sinuses with air in the orbit, air fluid levels in the ethmoid and maxillary sinuses on the right, and a fracture through the right optic foramen. There was no evidence of bony impingement of the right optic nerve (with coronal views), but the superior orbital fissure appeared distorted. The following day, a regimen of 8 mg of intravenous dexamethasone was instituted every eight hours. Nine days later, the patient underwent an obliteration and cranialization procedure, with an osteoplastic frontal sinus flap. Six weeks later, the patient's visual acuity, without correction, was R.E.: 2/200 and L.E.: 20/20. Color vision was impaired in the right eye (he could read none of the Ishihara color plates), but was normal in the left eye. Formal visual fields on a Goldmann perimeter showed a large central scotoma with a peripheral rim of preserved vision temporally and inferiorly (Fig. 6). He had a relative afferent pupillary defect and marked optic atrophy in the right eye.
Discussion
In these four patients, indirect injury to the optic nerve was the predominant cause of visu-
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Fig. 6 (Wolin and Lavin). Patient 4. Goldmann visual field examination performed six weeks after surgery shows partial recovery of the field of the right eye.
alloss. The first patient had no light perception in the left eye with an amaurotic dilated pupil that reacted consensually. The degree of hypherna and retinal edema did not account for the severity of visual loss. The second patient had no light perception in either eye, and his intraocular injuries were not sufficient to account for complete loss of vision. The third patient had no light perception in either eye when examined in the emergency room, but a few hours later, he had bare light perception in the left eye. Vision in the left eye began to recover before corticosteroids were introduced, and the further improvement might have been spontaneous. The surgical procedure involved reduction of nasal fractures, repair of the left orbital floor, and removal of an orbital bone spicule remote from the orbital apex; the optic nerve was not decompressed. The fourth patient also had some improvement in vision before the administration of corticosteroids. These patients are remarkable for the extent of recovery after the condition of no light perception. The first patient is also remarkable for the long interval between the head injury and recovery of vision, particularly in the absence of corticosteroid therapy. The optic nerve dysfunction in our patients may have been caused by transient failure of conduction (neuropraxia), edema, or transient ischemia of the optic nerve. In 1982, Anderson, Panje, and Cross" advocated the use of high-dose corticosteroids in traumatic optic neuropathy based on their experience with seven patients. Two patients recovered significant vision coincident with the use of corticosteroids, and two patients had a lesser degree of recovery, one after decompression of a subperiosteal orbital hematoma. Since then, there have been reports of similar suecesses,3,9-11 although Tang and associates," in a series of 37 patients, found corticosteroids un-
successful. Several recent studies have reported the lack of efficacy, indeed sometimes harmful effects, of corticosteroids in other neurologic disorders, including cerebral trauma." ischemic stroke," intracerebral hemorrhage," spinal cord injury.J'':" and acute polyneuropathy." The first patient recovered useful vision (from no light perception) with neither corticosteroids nor surgical intervention. The third and fourth patients began to recover vision before the initiation of corticosteroids. The second patient had some improvement soon after the introduction of corticosteroids, but had a prolonged interval between the injury and significant recovery of vision. Our patients received neither megadose corticosteroids nor hyperosmolar agents. A spontaneous recovery is frequently attributed to the introduction of therapy. Only a controlled randomized trial, or observations of definite deterioration on withdrawal of medication with subsequent recovery on re-introduction in a number of patients, will clarify the efficacy of corticosteroids. Such a controlled randomized trial, however, is probably not feasible." A number of reports 2,6,9,20,21 of successful decompression of traumatic optic neuropathy after optic nerve injury support the role of surgery, even when it is delayed as long as five days II; Spoor and Mathog describe such a patient who had a penetrating knife wound." Had our patients undergone decompressive surgery, the results would have been considered successful. When a compressive hematoma is present, the role of surgery seems clear; however, in the absence of such a hematoma, even with depressed bone fragments, the indications for surgery are less obvious. Whether a craniotomy with decompression of the optic nerve canal and falciform ligament is superior to the transethmoidal approach is also controversial." Re-
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ports of optic nerve decompression are difficult to evaluate because they are uncontrolled and not randomized. 2,6,8,9.2o.24 In the series of Fukado" and Niho, Niho, and Niho,23 the operative results were excellent; these studies, however, are criticizedv" for poor documentation and patient selection. Investigators, however, have found little benefit in optic nerve decompression in patients who have had immediate blindness caused by injury.2.12.24 Although a controlled randomized trial is probably not feasible, a central data bank for the accumulation and analysis of information on patients with indirect optic nerve injury may help clarify the management of this condition." The results of this study illustrate the potential for spontaneous recovery in patients with immediate blindness after injury and contradict the idea that an amaurotic pupil indicates irreversible visual loss." We believe that the only clear indication for surgical intervention in indirect optic nerve trauma, in the absence of a compressive lesion, is where visual loss initially improves with corticosteroid therapy and then repeatedly deteriorates with tapered doses.
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