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Show ORIGINAL CONTRIBUTION Traumatic Optic Neuropathy Caused by Blunt Injury to the Inferior Orbital Rim Tomo Nishi, MD, Tetsuo Ueda, MD, Eiichi Yukawa, MD, Takeo Ohta, MD, and Yoshiaki Hara, MD Abstract: A 48- year- old woman was struck on the right inferior orbital rim by a gardening device and immediately developed complete visual loss in the right eye. Clinical and imaging evaluations failed to disclose any damage to the globe or optic nerve or to their nearby soft tissues and bones. Within months, ipsilateral optic disc pallor, a nerve fiber bundle visual field defect, and a persistently subnormal visual acuity developed. We attribute the visual loss to indirect optic nerve injury. To our knowledge, blunt injury to the inferior orbital rim has not been reported as a cause of this phenomenon. (/ Neuro- Ophthalmol 2006; 26: 44- 46) Traumatic optic neuropathy ( TON) is most commonly caused by indirect injury through a blow to the superior orbital rim or brow that is transmitted through the bone to the optic canal where it contuses the optic nerve ( 1). We report a patient who developed optic nerve damage from a blow to the inferior orbital rim, a phenomenon not previously described. CASE REPORT A 48- year- old woman presented with sudden visual loss in the right eye. She had been weeding a garden and bending down when she was accidentally struck on the right inferior orbital rim by the obtuse top of a 10 mm diameter and 80 cm length stake used to support the growth of plants. The stake was made of steel and colored green so that it was difficult to recognize in the fields. She immediately noted rapid visual loss in the right eye and went to the hospital. On initial examination, visual acuity was no light perception ( NLP) OD and 20/ 15 OS. Intraocular pressures were 16 mmHg OD and 17 mmHg OS. In dim illumination, the pupil in the right eye measured 5 mm and the pupil in Department of Ophthalmology, Nara Medical University, Nara, Japan. Address correspondence to Tomo Nishi, MD, Department of Ophthalmology, Nara Medical University, 840 Shijo- chou, Kashihara City, Nara 634- 8522, Japan; E- mail: ntomo24@ r7. dion. ne. jp the left eye measured 3 mm. Both pupils were round; the pupil in the right eye did not react to direct light whereas the pupil in the left eye reacted normally; a relative afferent pupillary defect was present in the right eye. The anterior segment, ocular media, and fundus examinations were normal in both eyes ( Fig. 1). There was a superficial skin laceration of the lower lid at the orbital margin. Fluorescein angiography and indocyanine green angiography showed no delays in circulation time between arm and retina or between arm and choroid and no leakage from the optic discs or retinal blood vessels. Plain x- ray studies ( Waters, semi- Waters, Rhese methods) and CT of the head and orbits did not show any fractures ( Fig. 2). MRI showed no abnormalities of the optic nerves; neither optic nerve enhanced with contrast dye. As a result of these findings, we suspected TON. Therefore, we instituted a three- day course of intravenous methylprednisolone 1000 mg/ d followed by a tapering dose of oral prednisone over 11 days. One week after injury, visual acuity had improved to 20/ 200 in the right eye; one year after injury, it had improved to 20/ 100. The optic disc in the right eye had become diffusely pale at three months after injury while the optic disc in the left eye remained normal in appearance ( Fig. 1). Goldmann perimetery FIG. 1. One day after blunt trauma to the right orbit, the right optic disc appears normal ( left panel). Three months after injury, the right optic disc is diffusely pale ( right panel). 44 J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Inferior Orbital Rim Traumatic Optic Neuropathy J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 FIG. 2. Axial CT at the time of injury shows no soft tissue or bone abnormalities. showed a superior nerve fiber bundle defect at three months after the injury ( Fig. 3). DISCUSSION Most indirect injury to the optic nerve occurs from blows to the superior orbital rim or brow ( 1). Our case is unusual in that the blunt trauma appeared to affect the inferior orbital rim. We have excluded direct trauma of the optic nerve because: 1) the lid laceration in our patient was too superficial to suspect a penetrating injury with direct force on the optic nerve; 2) there were no indications of blunt injury to the globe itself; and 3) there was no imaging evidence of damage to the optic nerve or orbital soft tissues. However, the optic nerve was the site of damage, as it eventually became pale, a nerve fiber bundle visual defect appeared, and no abnormalities of the retina were found. We therefore assume that our patient suffered indirect injury to the optic nerve with a mechanism similar to that proposed for conventional indirect injury to the optic nerve. We have encountered no comparable reported cases except one by Laurence et al ( 2), in which injury to the nasal conjunctiva was associated with TON. The authors reported that the force of a merchandise display hook striking the left orbit nasally rotated the globe and caused optic nerve damage by stretching. As hypothesized by Leino ( 3), sudden stretching and tearing combined with compression and hemorrhage might be a major mechanism in optic nerve injury. The optic nerve is vulnerable to sudden stretching even without energetic co- forces or fractures. Sanborn et al ( 4) surmised that at least two mechanisms might be responsible for evulsion of the optic nerve after a non- penetrating injury ( 4). First, when struck by an / / X / J< M.- VL.- M > x l98pr> -" 1 *> -\ f 1 FV/ 4e | J Jtjftni ItMlYw 4 RAM. Int « n>. . Kwffl IiM! in':" hHl- FIC. 3. Three months after injury, Coldmann perimetry shows a large superior visual field defect in the right eye. 45 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Nishi et al object, the globe is displaced into the orbit, and intraocular pressure rises sharply, forcing the optic nerve away from the globe. Second, high intraorbital pressure forces the globe forward. A tethering effect results in separation of the optic nerve from the globe. We have considered a similar mechanism in our case. Furthermore, since the superior portion of the optic nerve is most tightly bound within the canal, the inferior pial vessels are considered to be most susceptible to shearing forces ( 1). Based on this hypothesis, the superior visual field would be lost, as in our case. Thus, a combination of optic nerve rotation and circulatory loss might conspire to cause visual loss. REFERENCES 1. Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv Ophthalmol 1994; 38: 487- 518. 2. Hou LC, Murphy MA. Traumatic optic neuropathy caused by a merchandise display hook. J Ped Ophthal Strab 2004; 41: 249- 50. 3. Leino M. Optic nerve injury after sudden traumatic rotation of the eye. Acta Ophthalmol 1986; 64: 364- 5. 4. Sanborn GE, Gonder JR, Goldberg RE, et al. Evulsion of the optic nerve: a clinicopathological study. Can J Ophthalmol 1984; 19: 10- 6. 46 © 2006 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. |
