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Traumatic Disruption of the Optic Chiasm

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Traumatic Disruption of the Optic Chiasm PHOTO ESSAY Traumatic Disruption of the Optic Chiasm Laura Segal, MDCM, Jella Angela An, MDCM, and Mark Gans, MDCM, FRCSC 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). Abstract: A 27-year-old man developed a persistent (J Neuro-Ophthalmol 2009;29:308–310) bitemporal hemianopia after severe head trauma sustained in a high-speed motor vehicle accident. The 27-year-old male pedestrian was hit by a car while he initial brain MRI revealed hemorrhagic contusion of Awas crossing the highway. The initial Glasgow Coma the optic chiasm. A brain MRI performed 4 weeks Scale score was 8 with reactive pupils bilaterally. Non- later demonstrated complete chiasmal transection, contrast brain CT revealed multiple bilateral orbital wall a phenomenon rarely documented with imaging. and facial fractures including the sphenoid walls, but there was no evidence of muscle entrapment or optic nerve sheath pathologic changes. McGill University Health Centre, Montreal, Quebec, Canada. Address correspondence to Laura Segal, MDCM, Montreal General Full ophthalmologic examination performed 5 days Hospital, 1650 Cedar Avenue, Montreal, QC H3G 1A4, Canada. E-mail: after the trauma disclosed a visual acuity of 20/50 in both [email protected] eyes. Pupils measured 4.5 mm in the right eye and 2.5 mm 308 J Neuro-Ophthalmol, Vol. 29, No. 4, 2009 Traumatic Disruption J Neuro-Ophthalmol, Vol. 29, No. 4, 2009 FIG. 2. Precontrast T1 coronal MRI shows traumatic midline cleft of the optic chiasm (arrow). (Modified from Gurses et al [10].) 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 FIG. 3. Gross (A) and histopathologic (B) specimens show ptotic. Results of slit-lamp examination and ophthalmos- a traumatic transection of the optic chiasm. (Modified from copy were unremarkable. Lindenberg et al [12].) 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 have sustained trauma to the cranial nerves, hypothalamus, consistent with intrinsic hemorrhage and edema of the and internal carotid artery (11). In one study, 68% had skull chiasm. Given that this finding would predispose to a fractures (21% frontal, 16% basal, and 31% frontal and compartment syndrome, a trial of high-dose corticosteroids basal). The others (32%) had closed head injuries, and the was initiated. However, the trial was discontinued the majority of these had subarachnoid and intracerebral following day because of evidence of a cerebrospinal fluid hemorrhages (11). Other findings have included cranial (CSF) fistula and the possibility of returning to the nerve deficits (anosmia, blindness, ocular motility defects, operating room for fistula repair. Four weeks later, brain and deafness), diabetes insipidus, CSF rhinorrhea, carotid- MRI showed complete longitudinal transection of the optic cavernous fistula, carotid aneurysm, meningitis, panhypo- chiasm (Fig. 1C). pituitarism, intrasellar hematoma, and pneumatocele Follow-up examination 8 weeks after the accident (5,6,9). Gurses et al. (10) reported a young man who revealed visual acuities of 20/30 in the right eye and 20/60 presented 4 months after severe head trauma with polyuria, in the left eye and no improvement in visual fields. polydipsia, anosmia, and constricted visual fields due to Abduction was still reduced in the left eye. Discs showed traumatic chiasmal syndrome (Fig. 2). mild pallor. Over the following 9 months, examinations Figure 3 provides a gross and histopathologic view of disclosed no further changes. a tear in the chiasm (12). The three proposed mechanisms Ever since the first description of traumatic chiasmal of such an injury include direct tearing, external compres- disruption by Nieden in 1883 (1), there have been only sion, and ischemic necrosis. a few reports (2–9). One study of 90 patients sustaining Direct shear injury of the optic chiasm is most often injuries to the visual pathway (2) revealed traumatic seen in severe central blows to the face (4). This proposed chiasmal injury in only 4.4%. Among the reported cases mechanism was initially rejected based on a study done on (2–9), only a handful of patients have shown complete cadaver models, which showed that the intracranial distance transection of the optic chiasm on imaging (4,5,8,9). between the optic foramina needs to be stretched from 12 to Traumatic injury to the optic chiasm occurs most 22 mm for the chiasm to be transected (13). Such a degree frequently when the impact is in the frontal area, usually of stretching was assumed to be an unlikely scenario for resulting in severe frontal head trauma accompanied by survivors of basilar skull fractures (5). However, using multiple cranial fractures (3,4,6,9,10). Survivors usually MRI, which allows clear visualization of the transected 309 J Neuro-Ophthalmol, Vol. 29, No. 4, 2009 Segal et al chiasm, it is understood that damage in vivo can range from REFERENCES micro-tears deep within the chiasm to complete sagittal 1. Nieden A. Zur Casuistik der nach traumat. Verletzungen des Hirns bisection in response to severe frontal impact (11). Such und Ruckenmarkes auftretenden Augenstorungen. Arch Augenheilk a direct mechanism of injury results in a permanent axonal 1883;12:30–52. 2. Hughes B. Indirect injury of the optic nerves and chiasma. Bull Johns injury at the moment of impact, and the visual deficit is Hopkins Hosp 1962;111:98–126. instantaneous and irreversible (11). 3. Tang RA, Kramer LA, Schiffman J, et al. Chiasmal trauma: clinical In contrast, indirect mechanisms can cause pro- and imaging considerations. Surv Ophthalmol 1994;38:381–3. 4. Mark AS, Phister SH, Jackson DE, et al. Traumatic lesions of the gressive damage to the optic nerve axons to develop hours suprasellar region: MR imaging. Radiology 1992;182:49–52. after the injury. The optic chiasm can be compressed either 5. Kawai K, Narita Y, Nagai A, et al. Traumatic chiasmal syndrome presenting with bitemporal hemianopsia. J Trauma 1998;44:224–9. by a downward herniation of the gyrus rectus (14) or via 6. Heinz GW, Nunery WR, Grossman CB. Traumatic chiasmal compression from hemorrhages surrounding the optic syndrome associated with midline basilar skull fracture. Am J chiasm (15). This process may occur without severe axonal Ophthalmol 1994;117:90–6. 7. Domingo Z, De Villiers JC. Post-traumatic chiasmatic disruption. Br injury, explaining the visual field recovery observed in J Neurosurg 1993;7:141–8. a few cases (13) and suggesting the need for early and 8. Sharma R, Goyal M, Sharma A, et al. Traumatic transection of the appropriate decompression. optic chiasm: magnetic resonance evaluation. Australas Radiol 1998; 42:80–2. Contusion necrosis, cited as the most common 9. De Nunzio M, McAuliffe W, Chakera TM. Magnetic resonance mechanism of chiasmal injury after head trauma (16), imaging of traumatic transection of the optic chiasm. Australas damages axonal neurons by secondary axotomy. Damage to Radiol 1997;41:155–6. 10. Gurses B, Selcuk H, Gokgoz T, et al. Traumatic transection of the the microcirculation of the intracanalicular optic nerve optic chiasm. Eur J Radiol Extra 2006;57:1–4. axons results in compressive edema (11). This process 11. Hassan A, Crompton JL, Sandhu A. Traumatic chiasmal syndrome: causes further compression of axons within the fixed a series of 19 patients. Clin Exp Ophthalmol 2002;30:273–80. 12. Lindenberg R, Walsh FB, Sacks JG. Neuropathology of Vision: An diameter of the bony optic canal, precipitating a positive Atlas. Baltimore: Lea and Febiger; 1973:221–3. feedback loop aggravated by an intracanalicular compart- 13. Savino PJ, Glaser JS, Schatz NJ. Traumatic chiasmal syndrome. ment syndrome (17,18). Neurology 1980;30:963–70. 14. Walsh FB, Gass JD. Concerning the optic chiasm: selected pathologic Because chiasmal trauma is rare, guidelines for its involvement and clinical problems. Am J Ophthalmol 1960;50:1031–47. management do not exist. Many studies have investigated the 15. Crompton MR. Visual lesions in closed head injury. Brain 1970;93: 785–92. use of high-dose intravenous corticosteroids and optic canal 16. Miller NR, Newman NJ. Walsh and Hoyt’s Clinical Neuro- decompression (19). However, results are conflicting and Ophthalmology: The Essentials. 5th ed. Baltimore: Williams & inconclusive. Therefore, most physicians make treatment Wilkins, 1998:134–8. 17. Tibbs PA, Brooks WH. Traumatic bitemporal hemianopsia: case decisions empirically. In one series of 19 patients by Hassan report. J Trauma 1979;19:129–31. et al (11), 15 (75%) were left with a visual acuity of 18. Joseph MP, Lessell S, Rizzo J, et al. Extracranial optic nerve 20/40 or better in at least one eye, as was the case in our decompression for traumatic optic neuropathy. Arch Ophthalmol 1990;108:1091–3. patient. However, 10 (50%) remained with no light per- 19. Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. ception in one eye. Cochrane Database Syst Rev 2007;4:CD006032. 310 q 2009 North American Neuro-Ophthalmology Society.
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