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Background: The prevalence of blindness as defined by law could be reduced by the introduction of anti-vascular endothelial growth factor (VEGF) therapy. Because the treatment is governed by patient needs, mostly using morphological criteria, imaging diagnostics are of particular importance. The non-interventional OCEAN study investigates the treatment with ranibizumab in the clinical routine practice. In a subgroup of patients the interpretation of spectral domain optical coherence tomography (SD-OCT) scans by the treating physicians will be analyzed (ORCA module)., Methods: Over a period of 24 months data from patients with exudative age-related macular degeneration (AMD), macular edema due to retinal vein occlusion or diabetes mellitus, who are receiving intravitreal injections of ranibizumab, will be assessed. Information on examinations, visual acuity, treatment and recordings from imaging techniques will be documented using a questionnaire. The SD-OCT scans, fluorescence angiography and fundus photography will be independently analyzed by the ophthalmologist of the study center and by three reading centers (CIRCL Cologne, GRADE Bonn and M3 Münster). Automated measurements of retinal thickness by the manufacturers' software will be checked and if necessary manually corrected. A qualitative interpretation in terms of morphological criteria for (further) treatment will be performed., Conclusion: A thorough assessment of SD-OCT images during anti-VEGF therapy provides the basis for the best possible needs-oriented treatment regimen. The control of the quality of data from daily routine practice may indicate possible weaknesses allowing explicit training and therefore optimization of patient treatment.

Background: Central retinal artery occlusion with persistent amaurosis as the only focal symptom caused by dissection of the internal carotid artery has occasionally been reported. Central retinal artery occlusion due to a common carotid artery dissection has been diagnosed only very rarely., Case Report: We describe a patient presenting with cervical pain, headache and unilateral amaurosis due to a thrombosis of the central retinal artery caused by a common carotid artery dissection, as demonstrated on MR imaging. No other neurological deficits could be detected. The patient underwent an anticoagulative treatment without improvement of his vision, but also without the appearance of further neurological symptoms., Conclusion: In monocular visual loss combined with cervical pain or headache, carotid artery dissection should be considered. Early treatment might be of crucial importance for the prevention of a devastating hemispheric stroke.

We report on two patients affected by Cogan's syndrome since infancy.Cogan's syndrome is described as the association of abrupt or intermittent worsening of vestibulo-auditory function and non-syphilic interstitial keratitis or, in patients with "atypical" Cogan's syndrome, various severe, inflammatory eye diseases. The first patient was affected with different inflammatory eye diseases from her fifth year and became blind in one eye when she was 7 years old. At that time, a deterioration of her hearing ability was also diagnosed. The hearing loss progressed to a severe hearing disorder. The second patient suffered from different inflammatory eye diseases from his second year. When he was 3 years old,he was diagnosed with a severe hearing disorder that progressed.Cogan's syndrome was diagnosed when he was 13 years old. The recognition of Cogan's syndrome is particularly complex in young patients. The difficulty of the diagnosis requires a search for ophthalmic diseases in young children with acute and progressive vestibulo-auditory symptoms.

History and Clinical Findings: A 15-year-old girl was admitted to hospital for acute bilateral visual deterioration and central scotoma of two days' duration. It became known on the third day that she had looked into the sun on several occasions, for several minutes at a time., Investigations: In addition to the scotoma there was a visual loss to 0.05 in the right and 0.1 in the left eye. Neurological examination and imaging of the head were unremarkable. At first the visual evoked potential was prolonged (122 ms on right, 130 ms on left), but all other electrophysiological tests were normal. Fundoscopy at first showed macular oedema and pigment changes in the macula., Treatment and Course: Local application of prednisolone (0.5 mg five times daily) gradually improved the vision and it returned to normal after 8 weeks. The initially prolonged visual evoked potential restored to normal either. No pathophysiological reason for this was found., Conclusion: In case of acute loss of vision in the absence of other neurological findings, external factors should be considered in the differential diagnosis.

Background: The bilateral simultaneous optic neuritis is rarely associated with multiple sclerosis. Diagnosis and prognosis have to be dealt with independently., Patient: A 45-year-old woman presented with an acute bilateral simultaneous amaurosis which developed within one day with bilateral papilledema. Initially there were positive antinuclear and anticytoplasmatic antibodies and antibodies against heart and skeletal muscles. The serum titer was elevated for immunoglobulin A, lowered for complement factors C3 and C4. Antigens for polio-virus type 3 and coxsackievirus type B5 and B3 were borderline positive. An oncologic, toxic or vascular cause of the neuritis was unlikely., Therapy and Course: The amaurosis lasted for 4 days. Vision improved gradually under a combined therapy with steroids, antibiotics and virostatics. Nineteen months later the vision was 20/25 OD and 20/200 OS., Conclusion: The acute bilateral neuritis was probably of autoimmunological origin. Under combined antiinfectious and steroidal therapy vision improved more than expected.

Objective: Presentation of the etiology, diagnosis, possible complications and treatment of amaurosis fugax., Definition: amaurosis fugax is a transient monocular loss of vision, usually affecting the entire visual field., Major Points: Amaurosis fugax is caused by transient retinal ischemia resulting from embolism, hemodynamic insufficiency or ocular vascular disease. In view of the high complication rate (annual blindness rate 1%, annual risk of an ischemic insult 2%, myocardial infarction 30%, and an 18% mortality rate), an immediate search for the underlying causes is mandatory. Diagnostic evaluation should include ophthalmological, neurological and cardiovascular investigations. Management of amaurosis fugax comprises, in the first instance, treatment of the underlying disease and administration of anti-platelet agents. In cases in which stenosis of extracranial vessels presents, endarterectomy may sometimes be considered.

For several months a 23-year-old woman had been suffering from increasingly frequent attacks of bilateral amaurosis fugax. They affected only individual segments of a monocular visual field and finally occurred several times daily. Physical and cardiological examinations as well as echocardiography were within normal limits. Laboratory tests revealed a slight increase in erythrocyte sedimentation rate and high titres of serum antibodies against phospholipids. Fundoscopy did not show any vascular changes. Because vasculitis--possibly as an expression of systemic lupus erythematodes--was suspected, high-dosage treatment with steroids was commenced, but failed to influence the visual disorder. While steroid dosage was gradually decreased, administration of acetylsalicylic acid (for three months 100 mg daily, then three times daily 100 mg) brought about complete disappearance of the visual signs. Their cause was probably a reversible platelet aggregation induced by antiphospholipid antibodies which, because of the physiological characteristics of the terminal retinal vascular bed brought about the isolated sign of recurrent amaurosis fugax.

After prolonged intake of oral contraceptives a 28-year-old woman developed a hemolytic uremic syndrome with microangiopathic hemolytic anemia, renal failure, malignant hypertension and blindness due to papillary congestion. Renal biopsy revealed widespread arteriolar alterations with massive intimal thickening, narrowing of the lumina and fibrinoid necrosis. During treatment with anticoagulation, antihypertensives and hemodialysis the hemolysis disappeared and vision improved, but the renal failure persisted. The possible relation between oral contraceptives and hemolytic uremic syndrome is mentioned and the literature is reviewed.