Approximately 1-2% of patients with defined SLE develop an optic<unk>  during the course of their disease. SLE-associated optic neuritis is rarely the presenting sign of the disease. The molecular pathogenesis is hypothesized, based on clinical features and the emerging understanding of mechanisms in SLE. Inflammation resulting from auto-antibodies, immune complexes, T-cells and complement, probably damages the components of the optic nerve, as well as the blood vessels (vasculitis). The resulting vasculitis causes a loss of blood supply to the nerve (ischemia). This combination of inflammation and ischemia may produce reversible changes such as demyelination alone, or more permanent damage axonal (necrosis), or a combination. The poor recovery of vision in AON despite anti-inflammatory treatment suggests that ischemia from the underlying vasculitis is an important component, but the details have not been established. It may be reasonable to consider that AON pathogenesis represents an incomplete expression of the SLE-associated optic<unk>  disease process.
Autoimmune optic neuropathy
Toxic and nutritional optic neuropathy
Arteritic anterior ischemic optic neuropathy
Chronic relapsing inflammatory optic neuropathy
Ischemic optic neuropathy
Posterior ischemic optic neuropathy
Retinal vasculitis
Autoimmune retinopathy