1Permanent visual loss occurs in an estimated 15% to 20% of patients with GCA. 2 The visual loss associated with GCA usually results from ischemic infarction of the optic nerve or retina 3,4 secondary to the vasculitic involvement of the posterior ciliary or central retinal arteries, respectively. 4 Patients with GCA may complain of a stuttering quality to their vision, an area of visual distortion, or the sudden and permanent loss of all or a portion of the vision in 1 or both eyes. In a retrospective study, premonitory visual symptoms occurred in approximately 65% of patients with subsequent permanent visual loss and included diplopia, amaurosis fugax, and visual blurring. 2 The onset of visual abnormalities antedated the onset of visual loss by an average of 8.5 days. Diplopia in association with GCA results from ischemia of extraocular muscles, cranial nerves, or the brain stem and may occur in up to 15% of patients with GCA. 5 When caused by localized extraocular muscle ischemia or cranial nerve infarction, the diplopia may resemble ischemic cranial mononeuropathy. It is therefore necessary to consider GCA in the differential diagnosis of patients with diplopia due to acute third, fourth, or sixth nerve palsies, especially when classic risk factors (diabetes, hypertension) are absent. Current Concepts in Diagnosis The evaluation of patients with suspected GCA and visual symptoms should include a detailed history, physical examination, and ophthalmologic evaluation. An urgent clinical examination of the patient with suspected GCA presenting with visual loss in 1 eye is especially important because the risk of visual loss in the contralateral eye is high. When bilateral involvement develops, the second eye is affected in 72% of patients within the first week after visual changes have occurred in the first eye. 6 The initial manifestations of GCA may be vague and nonspecific, including headache, malaise, weight loss, and fever. The diagnostic criteria of age of 70 years or older, new-onset headache, and abnormal temporal artery examination findings together have a sensitivity of 44% and a positive predictive value of 93% for GCA. These criteria plus jaw claudication decrease the sensitivity to 26.7% and increase the positive predictive value to 100%. 7 Although the superficial temporal arteries may be tender or nodular, 40% of patients with GCA will have clinically normal arteries. 8 In addition to measurement of visual acuity, the ophthalmologic examination should include assessment of the pupils for an afferent pupillary defect (possibly the only sign of posterior optic nerve infarction), ocular motility, and ophthalmoscopy of the retina and optic discs through dilated pupils. Ophthalmoscopic abnormalities are visible in more than 90% of patients with visual disturbances (Figure). Optic disc swelling secondary to ischemic optic neuropathy is seen in 70% to 80% of patients with visual loss associated with GCA. 3,4 Retinal cotton-wool