Permanent visual loss and cerebrovascular accidents in giant cell arteritis: predictors and response to treatment.

To assess the features and therapeutic response of visual manifestations and cerebrovascular accidents (CVA) in giant cell (temporal) arteritis (GCA) and to identify the predictors for permanent visual loss (VL) and CVA in GCA.,Two hundred thirty-nine patients with biopsy-proven GCA were included in a retrospective multicenter study. Data on demographic, clinical, and laboratory features were collected. The predictors were identified by a forward stepwise nonconditional logistic regression analysis.,Visual involvement was observed in 69 patients, and 34 had permanent VL. The diagnostic delay since the onset of visual symptoms was longer in the 11 patients with bilateral VL. The interval to involvement of the second eye was 5 days. The predictors of permanent VL were transient VL, jaw claudication, normal levels of liver enzymes, and absence of constitutional syndrome. Partial improvement of visual acuity was observed in 8 patients. After adjustment for the treatment regimen (intravenous pulse methylprednisolone versus oral prednisone), early treatment (within the first day of VL) was the only predictor of improvement. CVA, observed in 8 patients, involved the vertebral-basilar territory in 4. CVA was more frequent in patients with visual symptoms, appearing shortly after VL (median 7 days) and despite appropriate therapy. Predictors of CVA were permanent VL and jaw claudication.,In GCA, the risk of permanent VL is increased in patients with transient VL and/or jaw claudication, and decreased in those with elevated liver enzyme levels and/or constitutional syndrome. Partial therapeutic success is more probable if treatment is started within the first day of VL. CVA is more likely in patients with permanent VL and/or jaw claudication, often developing despite appropriate corticosteroid therapy.