Management of traumatic optic neuropathy--a study of 23 patients.

Abstract

Twenty three patients with traumatic optic neuropathy were managed by medical and surgical treatment as follows. High dose intravenous steroids were initiated in all patients. If visions did not improve significantly after 24 to 48 hours decompression of an optic nerve sheath haematoma by medial orbitotomy and neurosurgical decompression of the optic canal were considered based on computed tomographic scan findings. Nine of 16 patients who received steroids only showed significant improvement. One of three showed improvement on optic nerve decompression after steroid failure; three or four showed improvement with combined optic nerve sheath decompression by the medial orbitotomy and decompression of the optic canal by frontal craniotomy. A lucid interval of vision after injury and an enlarged optic nerve sheath were associated with an improved prognosis. Five of the 23 patients had a lucid interval and all five had a final improved vision, while only five of 18 patients without a lucid interval improved. Similarly seven of the nine with an enlarged optic nerve sheath showed improvement while only three of 10 patients (three bilateral cases) who presented with no light perception improved with medical and surgical treatment. While a prospective controlled study of the management of traumatic optic neuropathy is necessary this preliminary study suggests that treatment of traumatic optic nerve sheath haematoma by optic nerve sheath decompression should be considered in selected patients.Although the natural history of traumatic optic

High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial

“…This is similar to Levin's study [5], in which they concluded that initial visual acuity after trauma is a powerful prognostic factor in final visual acuity. This relation was also detected in other studies [9,11]. In our study, visual recovery in the first 48 h was a prognostic factor for final visual acuity.…”

Traumatic optic neuropathy in children and adolescents

“…1,4,5 Various options include high-dose [6][7][8] or low-dose 9 corticosteroids, immediate decompression of the canalicular portion of the optic nerve, 10 decompression of the canalicular optic nerve after a course of systemic corticosteroids, 11,12 observation, and optic nerve sheath fenestration in cases of anterior TON. 3 Unfortunately, findings in published reports have been inadequate to determine which, if any, of these treatments improves visual outcome after TON, mainly because of retrospective design, small numbers of matched cases, treatment bias, and unmasked outcomes.…”

Controversies in neuro-ophthalmology: Steroid therapy for traumatic optic neuropathy

“…Steroid therapy in TON has been examined in multiple case series, mostly nonrandomized, unblended and without controls. [ 4 5 ] The doses used in these trials can be categorized as follows: Moderate dose (60–100 mg of oral prednisolone), high dose (1 g of intravenous [IV] methylprednisolone/day), or megadose (30 mg/kg loading dose of IV methylprednisone, followed by 5.4 mg/kg/h for 24 h). The expected role of steroids has been in reducing inflammation and edema in the closed confines of the optic canal thereby preventing secondary compressive damage and providing neuroprotection by virtue of preventing free radical induced lipid peroxidation.…”