Both medical and surgical treatment has been proposed for the treatment of non-arteritic ischaemic optic neuropathy but, to date, no therapy is of significant benefit. Numerous drugs have been tried including anticoagulants, sub-Tenon's injections of vasodilators, intravenous noradrenaline (norepinephrine), thrombolytic agents, and corticosteroids. Johnson et al.92 reported that a combination of levodopa and carbidopa (Sinemet) prompted visual recovery in patients with non-arteritic AION of more than six months' duration. These results have not been confirmed. Haemodilution has also been described as improving visual function in longstanding non-arteritic AION93 and in AION of less than two weeks' duration when combined with pentoxifylline.94 Further verification of this potentially beneficial treatment is required. Direct surgical intervention by optic nerve sheath decompression has been shown in a multicentred randomised trial to be ineffective and possibly visually harmful.57 This type of surgery is no longer used in the United States.
The emergency treatment of choice in giant cell arteritis-associated AION or PION is high dose prednisone (60-80 mg per day) pending a temporal artery biopsy. Because of the risk to the second eye, this treatment is also recommended in suspected cases of giant cell arteritis in spite of a normal ESR or fibrinogen level. Corticosteroids in non-arteritic ischaemic optic neuropathy are of questionable value although they are frequently used when the second eye becomes involved. Embolic ischaemic optic neuropathy when symptomatic of ipsilateral ICA disease should be managed according to the severity of the carotid artery disease. (For additional guidance with regard to the management of retinal embolic disease, see "Branch retinal artery occlusion", the section "Emergency treatment".)
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