Abstract

To present a clinical series of 19 patients with traumatic chiasmal syndrome. A retrospective study was performed. This included all patients with traumatic chiasmal syndrome seen in the neuro-ophthalmology clinic at the Royal Adelaide Hospital between January 1970 and January 2000. Of the 19 study patients, most were young males involved in motor accidents. Two-thirds had skull fractures. Three-quarters of patients had a final visual acuity of 6/12 or better in at least one eye. Ten patients had a complete optic nerve palsy. The incidence of diabetes insipidus in this study was 37%. The incidence of cranial nerve lesions, hypopituitarism, carotid cavernous fistula, and other deficits were documented. Magnetic resonance imaging and surgical findings were consistent with known mechanisms of chiasmal injury. Trauma is a rare cause of chiasmal syndrome. Patients with bitemporal field defects should be questioned about prior head injury. In the acute setting, magnetic resonance imaging is the most useful investigation. The treating practitioner should anticipate and treat associated endocrine, ocular motility, and other disorders. Mechanisms of damage to the optic chiasm after trauma include direct tearing, contusion haemorrhage and contusion necrosis. These mechanisms should not be considered mutually exclusive. Unilateral temporal hemianopia with a fellow blind eye is not necessarily the result of chiasmal disruption.

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