Optic Neuritis

Optic neuritis is inflammation of the optic nerve, the structure that connects the eye to the brain. The optic nerve consists of nerve tracts (axons) that originate in the retina of each eye. The optic nerve carries visual information from the retina to the nerve cells in the brain stem, where the information is relayed to the area of the brain that recognizes vision (the occipital cortex).

Optic neuritis can occur in children or adults and may involve either one or both optic nerves. Optic neuritis typically affects young adults ranging from 18-45 years of age, with a mean age of 30-35 years. There is a strong female predominance. The annual incidence is approximately 5/100,000, with a total prevalence estimated to be 115/100,000.

The precise cause of optic neuritis is unknown, but it is thought to be a type of autoimmune disorder. The immune system is generally used to fight infection by creating a reaction that combats bacteria, viruses, fungi, and other foreign proteins. In autoimmune diseases, this reaction is mistakenly directed against a normal part of the body, creating inflammation and potential damage. In the case of optic neuritis, the optic nerve becomes swollen and its function is impaired. Inflammation of the optic nerve causes loss of vision because of the swelling and destruction of the protective myelin sheath that covers and insulates the optic nerve. Direct damage to the nerve tracts (axons) may also play a role in nerve destruction.

Optic neuritis most commonly develops due to an autoimmune disorder that may be triggered by a viral infection. In some people, signs and symptoms of optic neuritis may be an indication of multiple sclerosis, a disease in which the immune system attacks the myelin sheath covering nerve fibers in the brain and spinal cord, resulting in inflammation and damage to nerve cells in the brain and spinal cord. Demyelinating optic neuritis is another term for this eye condition. In optic neuritis resulting from demyelinating disease, particularly multiple sclerosis, there may be recurrences of optic neuritis over time.

In 15%-20% of people who eventually develop multiple sclerosis, optic neuritis is their first symptom. The risk of developing multiple sclerosis following one episode of optic neuritis is approximately 50% within 15 years of the episode of optic neuritis. On MRI scanning, almost half of the patients with optic neuritis (and no history or clinical evidence of multiple sclerosis) have abnormal brain white matter changes consistent with multiple sclerosis. In patients undergoing MRI scans of the brain at the time of the initial attack of optic neuritis, the finding of brain lesions on MRI images increased the risk of development of later multiple sclerosis threefold versus people with normal MRI scans. However, almost half of patients with any brain lesions on MRI at the time of the initial episode of optic neuritis will not have developed multiple sclerosis 10 years later.

Another autoimmune condition that causes optic neuritis is neuromyelitis optica. In this unusual condition, inflammation occurs in the optic nerve and spinal cord but usually not within the brain as often as in multiple sclerosis. Optic neuritis arising from neuromyelitis optica is more severe than optic neuritis associated with multiple sclerosis.

There are many causes of optic neuritis unassociated with multiple sclerosis, including:

• Infections: Bacterial infections, including Lyme disease, tuberculosis, cat scratch fever, toxoplasmosis and syphilis, or viral infections such as HIV (human immunodeficiency virus), hepatitis B, and herpes zoster can cause optic neuritis. Bacterial meningitis, encephalitis, and sinusitis (all especially in children) may cause optic neuritis or optic nerve damage.



• Cranial arteritis: This is an inflammation of the lining of the arteries within the skull. Inflamed cranial arteries can block blood flow to your eyes and brain, which may cause permanent vision loss or a stroke. Cranial arteritis is most likely to occur in adults 60-90 years of age. This condition is also known as temporal arteritis or giant cell arteritis (GCA).



• Diabetes: Diabetes is a condition in which the body cannot make or properly use insulin, a hormone that regulates the amount of sugar in the blood and other tissues. People with diabetes are at an increased risk of developing disorders of the optic nerve, including optic neuritis, most likely from decreased blood flow to the optic nerve.



• Sarcoidosis, pernicious anemia, Grave's disease, bee stings, and vaccinations may cause vision loss from optic nerve swelling.



• Autoimmune diseases (such as systemic lupus) may cause inflammation of blood vessels (vasculitis) nourishing the optic nerve.



• Drugs. Some drugs have been associated with the development of optic neuritis. These include ethambutol (Myambutol) and certain antibiotics.



• Toxins: Lead, methyl alcohol, quinine, and arsenic may cause vision loss and other symptoms that may mimic optic neuritis.



• Radiation therapy to the head is an uncommon cause of optic neuritis.



• Leber's hereditary optic neuropathy, an inherited form of vision loss that affects mostly males in their 20s or 30s, may cause optic neuritis.

However, the basic cause of optic neuritis is often unknown.

The term "optic neuropathy" is a more general term used to describe any condition that results in damage to the optic nerve. Optic neuritis is a specific type of optic neuropathy resulting from inflammation. Common noninflammatory causes of optic neuropathy include glaucoma, blocked or limited blood flow, direct trauma to the optic nerve(s), many neurological diseases, elevated intracranial pressure, primary and metastatic optic nerve tumors, nutritional deficiencies, and toxic exposure, including alcohol and tobacco, intraocular inflammation, and injuries. Trauma can interfere with the nerve's ability to conduct electrical impulses. All of these may cause vision loss and other symptoms that may mimic optic neuritis.

Source: MedicineNet.com
http://www.medicinenet.com/optic_neuritis/article.htm