The ischemic optic neuropathy is a Papilleninfarkt. The only symptom is painless vision loss. The diagnosis is made clinically. Treatments are not effective.
One distinguishes two types of Papilleninfarkts: Non-arteritic and arteritic. The non-arteritic variant is more common and usually affects people over age 50 and older. Vision loss is usually not as bad as in the arteritic variant which older and usually affects an older group of usually about 70 years.
The ischemic optic neuropathy is a Papilleninfarkt. The only symptom is painless vision loss. The diagnosis is made clinically. Treatments are not effective. One distinguishes two types of Papilleninfarkts: Non-arteritic and arteritic. The non-arteritic variant is more common and usually affects people over age 50 and older. Vision loss is usually not as bad as in the arteritic variant which older and usually affects an older group of usually about 70 years. Most of the ischemic optic neuropathy occurs unilaterally. At about 20% bilateral, temporally successive cases are observed, while a simultaneous bilateral disease is rare. Bilateral involvement is much more common in arteritic than non-arteritic cases. Atherosclerotic narrowing of the posterior ciliary arteries can lead to a non-arteritic optic nerve infarction, in particular after a Hypotoniephase. Any inflammatory arteritis, especially the giant (temporal arteritis) can trigger the arteritic form. Acute ischemia causes edema of the optic nerve, which further worsens the ischemia. A small Cup / disc ratio is a risk factor for a non-arteritic ischemic optic neuropathy, but not for the arteritic Art. Normally not a medical condition is found as the apparent cause of non-arteritic type, although factors that contribute to atherosclerosis ( eg. as diabetes, smoking, high blood pressure), obstructive sleep apnea, certain drugs (eg. as amiodarone, may phosphodiesterase-5 inhibitors) and hyperkoagulatorische disorders in some patients are suspected in place and as risk factors. The loss of vision when waking brought the investigators to the idea that nocturnal hypertension could be a possible cause of non-arteritic variant. Symptoms and signs The vision loss is in both species usually painless quickly (within minutes, hours or days) and. Some patients notice vision loss when you wake up. Symptoms such as general malaise, muscle pain, temporal headaches, painful hair brushes, jaw claudication and pain of temporal artery may occur along with Riesenzellenarteriitis; However, the symptoms can also occur after the loss of vision. Visual acuity is reduced and there is an afferent pupillary defect. The papilla is swollen and increased, and the swollen nerve fibers covering the surface of fine vessels of the optic nerve. The papilla is often surrounded by bleeding. The optic disc may be pale and congested in the non-arteritic form in the arteritic form. In both forms, the visual field examination often reveals a defect in the lower and central visual field. Diagnosis ESR, C-reactive protein and total blood count CT or MRI if the vision loss is progressive The diagnosis is mainly based on clinical judgment, but additional tests may be required. Most important is the exclusion of arteritic variant because the other eye is at risk, if the treatment is not initiated soon. Immediate tests include ESR, complete blood count and C-reactive protein. The ESR is usually increased dramatically in the arteritic form, normally in the non-arteritic form often more than 100 mm / h, and. A complete blood count is determined to identify thrombocytosis (> 400 x 103 / ul), which increases the positive and negative predictive content of a sole BSG. If giant cell arteritis is suspected, a biopsy of the temporal artery should as soon as possible be made (at least within 1 or 2 weeks because the effects of the prednisone treatment can reduce the diagnostic yield of histopathology). Changes in C-reactive protein are useful for monitoring disease activity and their response to treatment. In some cases a progressive visual loss pressure lesions should be ruled out by CT or MRI. In non-arteritic ischemic optic neuropathy, additional tests can be indexed based on the suspected cause or the suspected risk factor. If patients, for example, have excessive daytime sleepiness, or snoring or obesity, polysomnography should be considered for the diagnosis of obstructive sleep apnea be considered. If patients have vision loss when you wake up, 24-hour blood pressure monitoring can be performed. Prognosis There is no effective treatment for the arteritic variant, and the majority of vision loss can not be undone; in the non-arteritic form, however, up to 40% of patients recover spontaneously something useful vision. Treatment corticosteroids in the arteritic form. The arteritic form of oral corticosteroids treated (prednisone 80 mg p.o. 1 times a day and tapered off in consideration of the BSG) to protect the other eye. When a vision loss is imminent, should i.v. Corticosteroids are considered. Treatment should not be maintained pending the biopsy procedure or results. The treatment of non-arteritic form with aspirin or corticosteroids was ineffective. Risk factors are monitored. Low vision aids (eg. As magnifiers, large print devices, talking clocks) can be helpful in two ways. Tips and risks Give patients 55 years or older, have the sudden, painless loss of vision, as soon as possible systemic corticosteroids until a giant can be excluded. Summary Ischemic optic neuropathy is usually caused by giant cell arteritis or atherosclerosis. Ischemic optic neuropathy is suspected in patients aged 55 and older who have a sudden painless loss of vision. Unless it is excluded, the giant is treated to reduce the risk of contralateral involvement. The prognosis is usually poor. Enter corticosteroids when a giant comes into consideration.