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Show Joumal of Clinical Neuro- ophthalmology 8( 1): 9- 11,1988. f' 1988 Raven Press, Ltd" New York Evidence of Orbital Deformation In Indirect Optic Nerve Injury Weight Lifter's Optic Neuropathy Valerie Purvin, M. D. A 16- year- old boy developed monocular visual loss due to optic neuropathy following frontal head trauma, His trauma was unique in that it consisted of a static loading force to the brow, rather than the dynamic impact more commonly associated with blunt orbital injuries. This case demonstrates the role of isolated deformation of orbital bones in the pathogenesis of indirect optic nerve injury, Key Words: Mononuclear visual loss- Optic neuropathy- Trauma, From the Neuro- ophthalmology Section, Midwest Eye Institute, Indianapolis, Indiana, U. S. A. Address correspondence and reprint requests to Dr. Valerie Purvin, Neuro- ophthalmology Section, Midwest Eye Institute, 1800 North Capitol Avenue, Indianapolis, IN 46206- 1367, U. S, A, 9 Optic nerve injuries following head trauma can be divided into two groups: those associated with penetrating foreign bodies ( direct injury) and those caused by the force of impact remote from the site of trauma ( indirect injury) ( 1), In some cases, this impact fractures one or more orbital bones, with secondary laceration of the optic nerve or its vascular supply, In other cases, no such fracture is found, and the pathophysiology of optic nerve injury is more uncertain. Some cases of optic nerve injury have been caused by orbital hemorrhage ( 2), subperiosteal hematoma ( 3), or optic nerve sheath hemorrhage ( 4), but in many cases, the mechanism of injury remains speculative and is assumed to be a combination of mechanical disruption and ischemia. One theory favors tearing of the optic nerve at the canalicular entrance due to continued momentum of globe and nerve at the instant of sudden head deceleration ( 5). Another hypothesis invokes deformation of orbital bones, causing secondary vascular and neural injury ( 6). The following is an unusual case in which indirect optic nerve injury was due to pure deformation of orbital structures, without associated deceleration. CASE REPORT A 16- year- old boy was referred to the Indiana University neuro- ophthalmology service because of visual loss in the right eye. Earlier that day he had been bench- pressing a 270- lb barbell, when the weight gradually exceeded his muscular control, causing it to rest across his brow just above and to the right of the bridge of his nose. The event was witnessed by his trainer, who confirmed that the weight was gradually lowered onto the boy's forehead without any form of im- 10 V. PURVIN pact. Within 10- 15 s, the weight was removed by others in the room, following which the patient noted blurred vision in the right eye. His vision and general medical condition prior to this event had been unremarkable. On examination, best corrected visual acuity was 20/ 40 in the right eye and 20115 in the left. Color vision was intact, as determined by Ishihara pseudoisochromatic plates. Pupils were equal and reactive, with a right relative afferent defect. Goldmann perimetry in the right eye demonstrated a shallow cecocentral scotoma, containing a smaller area of absolute loss infero- temporal to fixation and mild constriction centrally. The left visual field was entirely normal ( Fig. 1). Ocular motility and slit lamp examinations were normat as was a dilated fundus exam. An orbital computed tomography ( CT) scan, including thin coronal sections through the optic canals, was entirely normal. Specifically, there was no evidence of fracture or hemorrhage. The patient was treated with prednisone, 100 mg/ day. He was reexamined 4 days later, at which time acuity had improved to 20115 in the right eye. The visual field had improved significantly, showing only a very small shallow central scotoma and mild constriction of the central isopter ( Fig. 2). Again, there was a right relative afferent pupillary defect and a normal fundus. Contrast sensitivity was reduced in the right eye at all spatial frequencies. His vision has been stable since that time. -- ". ~~ ". , '" TG <~.~.. 1M ...,. ,.", v_ e •• 1o~ Olh,,_ I I DISCUSSION The syndrome of indirect injury to the optic nerve has been known since the time of Hippocrates ( 7). The clinical picture is characterized by monocular visual loss following ipsilateral frontal or frontotemporal blunt trauma. Visual acuity is reduced to less than 20/ 200 in one- half of cases ( 8). Patterns of visual field loss are variable, inferior altitudinal defects being most common ( 9). Peripheral sector defects, generalized constriction, and centrat paracentrat or cecocentral scotomas may also occur ( 8). The optic disc appears normal acutely, with pallor developing from 4 days to 3 months later ( average 3 weeks) ( 5). The exact mechanism of such injury has remained speculative. Walsh studied the optic nerves of 70 patients who died from head trauma ( 10). He divided the pathologic changes he found into primary and secondary lesions. Primary lesions include hemorrhages into the optic nerve, dura, and sheath spaces, tears in the nerve and sheath, and contusion necrosis. Secondary lesions include optic nerve edema, necrosis from systemic circulatory failure or local compression of vessels, and infarction related to vascular obstruction. He noted that the nerves were most often and most severely damaged at their entry into the optic canal and in the intracanalicular segment. This pattern of injury was also found by Edmund and Godtfredsen ( 5), who noted that the firm attachment of the dural sheath to the optic nerve in the -~ .30 fGc ....~'.......... '-"'< 1_"' Io~ O'''''_ I I FIG. 1. Goldmann visual fields several hours after injury. There is mild constriction and a relative cecocentral scotoma in the right eye. The left visual field is normal. ,.. . w:.: ,:,;:~,,:,,::: .-::....... I I OPTIC NERVE INJURY 30' I I 30' ')) 0 JJ FIG. 2. Goldmann perimetry 4 days after injury showing only a small shallow central scotoma and some constriction of central isopters in the right eye. upper part of the canal makes this region particularly susceptible to such injury. One proposed mechanism holds that at the moment of impact, the globe and intraorbital optic nerve continue their forward movement, resulting in tears at the entrance to the canal where the nerve is tethered. Such tears may involve the nerve directly or the nutrient dural vessels that nourish the nerve, thus leading to hemorrhage and/ or infarction. Anderson et al. ( 6) proposed an alternate mechanism for indirect optic nerve injury. In their experimental model, static forces were applied to the facial eminences of dried human skulls. The pattern and degree of deformation of skull bones were recorded by means of holographic interferometry. Forces applied to the supra- orbital ridge produced maximum stress concentration in the orbital roof about 5- 8 mm from the optic foramen. Based on this data, they postulated that indirect optic nerve injury is due, at least in part, to deformation of orbital bones at the time of impact. As cases of indirect injury to the optic nerve typically involve a blow to the frontal region, the relative contributions of orbital deformation and sudden deceleration are difficult to separate. The case presented here is unusual because no impact occurred during the injury. This patient's optic nerve trauma thus represents the clinical equivalent of Anderson's in vitro holography experiments. We believe our patient's visual loss was due to distortion of the optic canal by a force applied to the supra- orbital ridge, causing damage to the intracanalicular optic nerve. Damage to the optic nerve may have been due to a small hemorrhage into the nerve, which was perhaps induced by the extreme valsalva maneuver undoubtedly executed by the patient during the course of his weight lifting or an area of contusion secondary to the orbital deformation. Treatment with steroids may have been responsible for the prompt improvement of vision by reducing local swelling or such recovery may have been coincidental. REFERENCES 1. Battle WHo Lectures on some p,' ints rl'lated to injuries t" the head. Lallcc/ 1890; 11: 57- 63. " 1 Katz B. Herschler j. Brick DC. Orbital haeml1rrhage and prolonged blindness: a treatable poskri,' r ,' ptiC neuropathy. Br I Ophtllll/ II/ ll/ 1983; 67: 549- 53. 3 Gill'um INN. Andl.' rSlln RL. Rl'\' l'rsibk \' isual Inss in subperiosteal hematllIna uf till' orbit. 0l'hI1l, I/ IIl/( SIII'S 1981.12: 203- 9. 4. Pringle JH. tv1< lmlcular blindness f,' llll\\' ing diffuse \' iolem: e to the skull: its causatilll1 and treatment. Br I SlIr" 1916- 1917; 4: 373- 85. ' 5. Edmund J. Glldtfredsen E. Unilateral optic atrophy folloWing head inJury. Actll 01' 11/ 1111/ 11/( 1/ 1963;- 11: 693- 7. 6. Andl.' rsnn RL. P, 1I1je WR, Gross CEo Optic ner\' e blindness following blunt forehead trauma. 01' 1IIh' 1/ 1l1( l/ oSlf 1982; 89: 445- 55. 7. Chadwick J. Mann WN. The Illediml ,('( 1/' ks or Hil'l'( lcralcs. Oxford. England. Blackwell. 1950. 8. Turner JWA. Indirect injuries of the' optic nerve. Bmil! 19- 13; 66: l- lL)- 51. 9. Hughes B. Indirect injury of the llptiC nerve and chiasm. Bull / ohlls Hopkills Hosp 1962; 111: 98- 126. 10. Walsh FB. Palholugical- dinical clHrelations. I. Indirect trauma to the optic nerves and chiasm, Il. Certain cerebral involvements ass() ciated with detective blood supplv. 111_ ltest 0l'htIIll11l1( l/ 1966; 5: 433-- I9. ~ J Clill N" lIro- l'plttllllll/ lol, Vol. 8. N, l. J, 1988 [VBtraumaticvisualloss] |
