Giant cell arteritis dementia and other steroid-responsive dementia syndromes are a unique opportunity for clinicians and researchers.

When evaluating patients with dementia, it is common to check for easily reversible problems, such as hypothyroidism, normal pressure hydrocephalus and B12 deficiency. Although these are not usually the main cause of a patient's troubles, correcting them improves chances for preserving, or at least stabilising, cognitive status. This letter makes the argument that both clinicians and researchers should give more attention to looking for giant cell arteritis (GCA) and other steroid-responsive conditions, as a routine part of the standard dementia workup. GCA is the most common cerebral vasculitis among the elderly of European ancestry, with an incidence on the order of 1–10 per 100,000. The prevalence of GCA in other ethnic populations is not well known, but in one survey in Japan, prevalence was estimated at one per 100,000. It was once believed that GCA did not exist in China or India, but verified cases have been documented over the past two decades; a recent report suggests that the incidence of GCA in China might be significantly underestimated. Similarly, it is thought that among African-Americans in the United States, there might be many occult, unrecognised cases of GCA. The typical GCA presentation is an elderly patient with headaches or visual loss, an elevated sedimentation rate, associated symptoms of proximal muscle stiffness (polymyalgia rheumatica), anaemia and a temporal artery biopsy showing giant cell arteritis. GCA is treated with high dose corticosteroids (prednisone 60 mg per day, prednisolone or intravenous solu-medrol at comparable potencies). Steroids are continued for many months with a very gradual tapering. Proof-of-principle that dementia caused by occult, unrecognised GCA, that otherwise might be written off as typical Alzheimer's disease or vascular dementia, can be established from published case histories. For example, in 2005, a 76-year-old man presented with acute right-sided periocular pain and diminished vision. He had a sedimentation rate of 73 mm/hr, cilioretinal artery occlusion and " florid " GCA seen on temporal artery biopsy. He was quite impaired cognitively, but prednisolone 50 mg per day produced rapid normalisation of his mental status, and at that point, his family commented that he had actually had dementia for at least a few years. Further investigation revealed that three years before, he had suffered a right-sided middle cerebral artery stroke that had been accompanied by scalp tenderness and right-sided headache. A diagnosis of GCA had been considered at that time but was not pursued because sedimentation rate was only …