Traumatic Optic Neuropathy: Update on Management

Traumatic Optic Neuropathy: Update on Management: Comparison

Please note this is a comparison between Version 2 by Rita Xu and Version 1 by Mohammad Reza Hosseini Siyanaki.

Traumatic optic neuropathy is one of the causes of visual loss caused by blunt or penetrating head trauma and is classified as both direct and indirect. Clinical history and examination findings usually allow for the diagnosis of traumatic optic neuropathy. There is still controversy surrounding the management of traumatic optic neuropathy; some physicians advocate observation alone, while others recommend steroid therapy, surgery, or both. In this entry, we tried to highlight traumatic optic neuropathy’s main pathophysiologic mechanisms with the most available updated treatment. Recent research suggests future therapies that may be helpful in traumatic optic neuropathy cases.

Traumatic optic neuropathy is one of the causes of visual loss caused by blunt or penetrating head trauma and is classified as both direct and indirect. Clinical history and examination findings usually allow for the diagnosis of traumatic optic neuropathy. There is still controversy surrounding the management of traumatic optic neuropathy; some physicians advocate observation alone, while others recommend steroid therapy, surgery, or both. In this entry, researchers tried to highlight traumatic optic neuropathy’s main pathophysiologic mechanisms with the most available updated treatment. Recent research suggests future therapies that may be helpful in traumatic optic neuropathy cases.

optic nerve
traumatic optic neuropathy
corticosteroids therapy
surgical management

Traumatic optic neuropathy (TON) is a grave complication of closed head injury. It occurs in 0.7–2.5% of the population and is classified into direct and indirect TON ^[1].

Direct TON often results in complete vision loss and less chance of recovery than indirect TON. Direct TON usually occurs after bone fragments lacerate the optic nerve or when a concussion or contusion disrupts the optic nerve [2,3]^[2][3]. However, indirect TON usually develops due to blunt head or ocular trauma sustained via the oculofacial soft tissues and skeletal system to the optic nerve ^[4]. The visual loss may manifest several months after trauma; therefore, the diagnosis is always delayed ^[5]. TON management remains controversial; some physicians advocate observation alone, while others recommend high-dose corticosteroids, surgical optic canal decompression, or a combination. In this review entry, weresearchers try to highlight the main updates involving the management of TON.

References

Karimi, S.; Arabi, A.; Ansari, I.; Shahraki, T.; Safi, S. A systematic literature review on traumatic optic neuropathy. J. Ophthalmol. 2021, 2021, 5553885.
Atkins, E.J.; Newman, N.J.; Biousse, V. Post-traumatic visual loss. Rev. Neurol. Dis. 2008, 5, 73.
Cirovic, S.; Bhola, R.M.; Hose, D.R.; Howard, I.C.; Lawford, P.V.; E Marr, J.; A Parsons, M. Computer modelling study of the mechanism of optic nerve injury in blunt trauma. Br. J. Ophthalmol. 2006, 90, 778–783.
Sarkies, N. Traumatic optic neuropathy. Eye 2004, 18, 1122–1125.
Yu-Wai-Man, P.; Griffiths, P.G. Steroids for traumatic optic neuropathy. Cochrane Database Syst. Rev. 2013, 6, CD006032.