The optic nerve is a bundle of millions of fibers in the retina that sends visual signals to the brain.
Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy.
Ischemic optic neuropathies are classified based on the location of the damage and the cause of reduced blood flow if known.
Presence of an afferent pupillary defect, decreased color vision, and visual field loss (often central) are suggestive of optic neuritis.
Tumors, infections, and inflammatory processes can cause lesions within the orbit and, less commonly, the optic canal.
Patients often have bulging out of the eye (proptosis) with mild color deficits and almost normal vision with disc swelling.
Indirect injuries, like blunt trauma to the forehead during a motor vehicle accident, transmit force to the optic nerve without transgressing tissue planes.
This type of force causes the optic nerve to absorb excess energy at the time of impact.
The role of high-dose steroids and orbital decompression in treating these patients is controversial and, if administered, must be done very soon after injury with minimal effects.
Mitochondria play a central role in maintaining the life cycle of retinal ganglion cells because of their high energy dependence.
Mitochondria are made within the central somata of the retinal ganglion cell, transported down axons, and distributed where they are needed.
[5] A nutritional optic neuropathy may be present in a patient with obvious evidence of under-nutrition (weight loss and wasting), but also malnutrition due to picky eating as in autism.
While optic neuropathy cannot be outright cured, there are surgical options to alleviate pain and symptoms associated with such diseases.