Traumatic optic neuropathy therapy: an update of clinical and experimental studies.

Abstract

Serious injury to the optic nerve, including direct and indirect events, induces significant visual loss and even blindness. For the past decade corticosteroids and/or optic canal decompression surgery have been widely embraced therapeutic paradigms for the treatment of traumatic optic neuropathy. There is little clinical evidence, however, to support the effectiveness of these strategies, raising questions about the efficiency of current therapy for improving visual outcomes. Recently, experimental studies have yielded a wealth of information related to the protection and regeneration of retinal ganglion cells, showing promise for the development of novel and effective treatments for optic nerve injury.

• Authors: N Wu, Z Q Yin, Y Wang
• Journal: The Journal of international medical research (J Int Med Res) 2008 Sep-Oct Vol. 36 Issue 5 Pg. 883-9 ISSN: 0300-0605 [Print] England
• PMID: 18831880 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Crystallins
• Nerve Growth Factors
• Steroids
• Tumor Necrosis Factor-alpha
• Nitric Oxide
• Glutamic Acid

Topics

• Animals
• Blindness (etiology)
• Clinical Trials as Topic
• Crystallins (metabolism)
• Decompression, Surgical
• Glutamic Acid (metabolism)
• Humans
• Nerve Growth Factors (metabolism)
• Nitric Oxide (metabolism)
• Optic Nerve (drug effects, pathology, physiology, surgery)
• Optic Nerve Diseases (etiology, pathology, therapy)
• Optic Nerve Injuries (complications, pathology, therapy)
• Retinal Ganglion Cells (metabolism, pathology)
• Steroids (therapeutic use)
• Tumor Necrosis Factor-alpha (metabolism)