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Show PHOTO ESSAY Traumatic Disruption of the Optic Chiasm Laura Segal, MDCM, Jella Angela An, MDCM, and Mark Gans, MDCM, FRCSC Abstract: A 27- year- old man developed a persistent bitemporal hemianopia after severe head trauma sustained in a high- speed motor vehicle accident. The initial brain MRI revealed hemorrhagic contusion of the optic chiasm. A brain MRI performed 4 weeks later demonstrated complete chiasmal transection, a phenomenon rarely documented with imaging. ( J Neuro- Ophthalmol 2009; 29: 308- 310) A 27- year- old male pedestrian was hit by a car while he was crossing the highway. The initial Glasgow Coma Scale score was 8 with reactive pupils bilaterally. Non-contrast brain CT revealed multiple bilateral orbital wall and facial fractures including the sphenoid walls, but there was no evidence of muscle entrapment or optic nerve sheath pathologic changes. Full ophthalmologic examination performed 5 days after the trauma disclosed a visual acuity of 20/ 50 in both eyes. Pupils measured 4.5 mm in the right eye and 2.5 mm FIG. 1. A. Goldmann visual field examination demonstrates complete bitemporal hemianopia. B. T2 coronal MRI performed on the day of the accident reveals enlargement and distortion of the optic chiasm, with high signal mostly on the left side due to intrinsic hemorrhage ( arrow). C. T2 coronal MRI performed 4 weeks after the accident reveals thickening and distortion of the chiasm and complete transection on the left side ( arrow). McGill University Health Centre, Montreal, Quebec, Canada. Address correspondence to Laura Segal, MDCM, Montreal General Hospital, 1650 Cedar Avenue, Montreal, QC H3G 1A4, Canada. E- mail: lsegal2@ gmail. com 308 J Neuro- Ophthalmol, Vol. 29, No. 4, 2009 in the left eye without relative afferent pupillary defect. Visual fields by confrontation revealed a complete bitem-poral hemianopia, which was later confirmed by Goldmann perimetry ( Fig. 1A). There was substantially reduced infraduction of the right eye and abduction of the left eye, resulting in binocular diplopia. The right upper lid was ptotic. Results of slit- lamp examination and ophthalmos-copy were unremarkable. Orbit MRI revealed an enlarged and distorted optic chiasm with normal optic tracts and optic nerve sheath complexes ( Fig. 1B). These MRI findings were most consistent with intrinsic hemorrhage and edema of the chiasm. Given that this finding would predispose to a compartment syndrome, a trial of high- dose corticosteroids was initiated. However, the trial was discontinued the following day because of evidence of a cerebrospinal fluid ( CSF) fistula and the possibility of returning to the operating room for fistula repair. Four weeks later, brain MRI showed complete longitudinal transection of the optic chiasm ( Fig. 1C). Follow- up examination 8 weeks after the accident revealed visual acuities of 20/ 30 in the right eye and 20/ 60 in the left eye and no improvement in visual fields. Abduction was still reduced in the left eye. Discs showed mild pallor. Over the following 9 months, examinations disclosed no further changes. Ever since the first description of traumatic chiasmal disruption by Nieden in 1883 ( 1), there have been only a few reports ( 2- 9). One study of 90 patients sustaining injuries to the visual pathway ( 2) revealed traumatic chiasmal injury in only 4.4%. Among the reported cases ( 2- 9), only a handful of patients have shown complete transection of the optic chiasm on imaging ( 4,5,8,9). Traumatic injury to the optic chiasm occurs most frequently when the impact is in the frontal area, usually resulting in severe frontal head trauma accompanied by multiple cranial fractures ( 3,4,6,9,10). Survivors usually have sustained trauma to the cranial nerves, hypothalamus, and internal carotid artery ( 11). In one study, 68% had skull fractures ( 21% frontal, 16% basal, and 31% frontal and basal). The others ( 32%) had closed head injuries, and the majority of these had subarachnoid and intracerebral hemorrhages ( 11). Other findings have included cranial nerve deficits ( anosmia, blindness, ocular motility defects, and deafness), diabetes insipidus, CSF rhinorrhea, carotid-cavernous fistula, carotid aneurysm, meningitis, panhypo-pituitarism, intrasellar hematoma, and pneumatocele ( 5,6,9). Gurses et al. ( 10) reported a young man who presented 4 months after severe head trauma with polyuria, polydipsia, anosmia, and constricted visual fields due to traumatic chiasmal syndrome ( Fig. 2). Figure 3 provides a gross and histopathologic view of a tear in the chiasm ( 12). The three proposed mechanisms of such an injury include direct tearing, external compres-sion, and ischemic necrosis. Direct shear injury of the optic chiasm is most often seen in severe central blows to the face ( 4). This proposed mechanism was initially rejected based on a study done on cadaver models, which showed that the intracranial distance between the optic foramina needs to be stretched from 12 to 22 mm for the chiasm to be transected ( 13). Such a degree of stretching was assumed to be an unlikely scenario for survivors of basilar skull fractures ( 5). However, using MRI, which allows clear visualization of the transected FIG. 2. Precontrast T1 coronal MRI shows traumatic midline cleft of the optic chiasm ( arrow). ( Modified from Gurses et al [ 10].) FIG. 3. Gross ( A) and histopathologic ( B) specimens show a traumatic transection of the optic chiasm. ( Modified from Lindenberg et al [ 12].) 309 Traumatic Disruption J Neuro- Ophthalmol, Vol. 29, No. 4, 2009 chiasm, it is understood that damage in vivo can range from micro- tears deep within the chiasm to complete sagittal bisection in response to severe frontal impact ( 11). Such a direct mechanism of injury results in a permanent axonal injury at the moment of impact, and the visual deficit is instantaneous and irreversible ( 11). In contrast, indirect mechanisms can cause pro-gressive damage to the optic nerve axons to develop hours after the injury. The optic chiasm can be compressed either by a downward herniation of the gyrus rectus ( 14) or via compression from hemorrhages surrounding the optic chiasm ( 15). This process may occur without severe axonal injury, explaining the visual field recovery observed in a few cases ( 13) and suggesting the need for early and appropriate decompression. Contusion necrosis, cited as the most common mechanism of chiasmal injury after head trauma ( 16), damages axonal neurons by secondary axotomy. Damage to the microcirculation of the intracanalicular optic nerve axons results in compressive edema ( 11). This process causes further compression of axons within the fixed diameter of the bony optic canal, precipitating a positive feedback loop aggravated by an intracanalicular compart-ment syndrome ( 17,18). Because chiasmal trauma is rare, guidelines for its management do not exist. Many studies have investigated the use of high- dose intravenous corticosteroids and optic canal decompression ( 19). However, results are conflicting and inconclusive. Therefore, most physicians make treatment decisions empirically. In one series of 19 patients by Hassan et al ( 11), 15 ( 75%) were left with a visual acuity of 20/ 40 or better in at least one eye, as was the case in our patient. 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