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The most common cause of traumatic optic neuropathy (TON) is indirect injury to the optic nerve, which is thought to be the result of transmitted shock from an orbital impact to the intracanalicular portion of optic nerve. Direct TON can result from penetrating injury or from bony fragments in the optic canal or orbit piercing the optic nerve. Orbital hemorrhage and optic nerve sheath hematoma can also cause TON by direct compression. There may be optic nerve avulsion and transection also. Trauma to the optic nerve rarely improves vision with best of the management. The diagnosis of TON is made clinically based on history and ophthalmic signs along with neurological investigations. The management of indirect optic nerve injury is controversial. Experimental studies of optic nerve injury have employed Corticosteroid Randomization After Significant Head injury study, National Acute Spinal Cord Injury Study (NASCIS 2 and 3) and optic canal depression surgery. Most of the therapeutic regimens have been extrapolated from the NASCIS II, which showed a statistically significant improvement in neurologic outcome (motor and sensory) in a subgroup analysis of acute spinal cord injury patients receiving a methylprednisolone 30 mg/kg bolus within 8 h of injury, followed by 5.4 mg/kg/h for 23 h, but sometimes have high death rates and other complications. Based on the studies, good results can be obtained if interventions are made within 8 h of incident and observation thereafter.