Optic nerve damage in head trauma: clinical and experimental studies.

A total of 33 cases with optic nerve damage due to blunt head trauma were followed for 6 months to one year with the average follow-up period of 9 months. Eleven cases were treated by surgical decompression of the optic canal and 22 cases were followed by medical treatment. The optic canal fracture was documented in 51% of the cases, and the incidence was not significantly different between both groups. When the visual acuity was zero at the time of the first examination, no visual improvement could be obtained. Omitting these cases, visual improvement was seen in 42.8% of patients treated by surgery and in 58.8% of patients with medical treatment, which consisted of a combined use of prednisolone, mannitol, urokinase and vitamin B12. The percentage of visual improvement did not differ between cases with and without optic canal fracture. In the Japanese monkey, the optic nerve was exposed and various insults were given, including traction, ligation and small optic sheath resection. After traction and ligation, the visually evoked response (VEP) became extinguished or reduced, but after release from the insult, a tendency of recovery was found in the VEP. The threshold to elicit the VEP by localized light stimulus was increased by optic nerve ligation, but after its release the threshold tended to decrease. The effects of the optic nerve sheath resection were slight, and the increase in the threshold recovered after 4 weeks. It was thought that the optic nerve is resistant to indirect insults. From the clinical and experimental studies, it was concluded that the mechanism of the optic nerve damage due to blunt head trauma is multiple, and that the cases should be treated by intensive medical treatment rather than by surgical intervention.