A 52‐year‐old man with a history of psoriasis presented with a 1‐week of gradually worsening and throbbing headache over both his temples. He found little relief from nonsteroidal anti‐inflammatory drugs, and his headache was different from prior headaches. The pain did not radiate. He did not experience any neck pain, photophobia, phonophobia, rigors, weight loss, nausea, vomiting, tinnitus, rhinorrhea, jaw claudication, or muscle pain. He did, however, report subjective fever, diplopia, episodes of blurry vision, and vision loss in both eyes that began 1 week prior to presentation. He had equally reactive pupils, full visual fields, no gaze palsy. Strength and sensation were intact throughout. The temporal arteries were visibly engorged with 2+ pulses and exquisite tenderness. No carotid bruits were auscultated. Peripheral pulses were full in the distal extremities. There were no murmurs on the cardiac exam. The erythrocyte sedimentation rate (ESR) was 14 mm/hour, and his other labs were unremarkable. There was no evidence of intracranial bleeding or stroke seen on CT or MRI. Carotid artery ultrasonography revealed no evidence of stenosis. He was started on 1 mg/kg of oral prednisone for temporal arteritis. The patient did not attend his outpatient appointment for a planned temporal artery biopsy.
Headache is a very common presenting complaint encountered by the hospitalist; thus, a systematic method is required. One method is to envision the head as an egg, and by working from the skin and soft tissue, through the skull and meninges, to the brain parenchyma, identifying all the causes of headache. This patient had significant abnormalities in his temporal arteries. These physical exam findings combined with his age and new headache were specific for a diagnosis of temporal arteritis. Temporal arteritis is an autoimmune disease of unknown etiology. It is postulated that an initial factor, which may be viral in origin, binds with monocytes, activating them. The monocytes produce inflammatory cytokines causing symptoms of fever and malaise and raising the ESR. However, approximately 5%–10% of patients have a normal ESR, and this correlates with a lack of systemic symptoms, but an equal occurrence of ischemic symptoms. Activated monocytes then invade portions of the adventitia of large arteries via the vasa vasorum and differentiate into macrophages. There, the macrophages encounter circulating antigens and produce cytokines including interferon gamma, which result in the recruitment of additional macrophages, and create narrowing, fibrosis, and scarring of the arteries. In addition, this inflammation can cause thrombosis of the arteries, leading to ischemia of the skin and soft tissue, as well as acute visual loss.
Given the visual complications of untreated temporal arteritis, physicians should have a low index of suspicion for temporal arteritis and assuaged by a normal ESR.
To cite this abstract:Cerreta K, Barnes M, Price A. A Blinding Headache. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 229. Journal of Hospital Medicine. 2013; 8 (suppl 2). https://www.shmabstracts.com/abstract/a-blinding-headache/. Accessed November 22, 2019.