Temporal arteritis is a condition where the immune system attacks the walls of medium and large arteries, most commonly the arteries running along the temples. Also called giant cell arteritis (GCA), it’s the most common form of blood vessel inflammation and occurs almost exclusively in people over 50, with a median age of diagnosis around 75. Left untreated, it can cause permanent vision loss in roughly 1 in 5 patients.
What Happens Inside the Arteries
The disease starts in the outer layer of the artery wall, where immune cells called dendritic cells become abnormally activated. These cells send out chemical signals that recruit waves of additional immune cells, particularly a type of white blood cell called T-cells, into the artery wall. Those T-cells then trigger macrophages (the immune system’s cleanup crew) to multiply and cluster together, forming what are called “giant cells,” which is where the condition gets its formal name.
This chain reaction causes the artery wall to thicken and swell from the inside, narrowing the channel that blood flows through. In some cases, the vessel can become completely blocked. Because the temporal arteries supply blood to the head and eyes, this narrowing is what produces the headaches, scalp pain, and vision problems that define the condition.
Who Gets It
Temporal arteritis is most common in white Northern European populations and affects women more often than men. In one study from Sheffield, England, over 94% of patients investigated for the condition were white British or Irish. Other ethnic groups accounted for small minorities: about 1.7% Asian or Asian British, 1.7% Black or Black British, and 1.1% other backgrounds. That said, GCA can occur in any ethnic group, and the condition may simply be underdiagnosed in non-white populations.
Between 40% and 60% of people diagnosed with temporal arteritis also have polymyalgia rheumatica (PMR), a related condition that causes aching stiffness in the shoulders, hips, and neck, especially in the morning.
Symptoms to Recognize
A new, persistent headache centered at the temples is the hallmark symptom, appearing in 60% to 90% of confirmed cases. The headache often feels different from any headache you’ve had before. It may be one-sided or affect both temples, and the scalp in that area can become so tender that brushing your hair or resting your head on a pillow is painful.
Jaw claudication is the most distinctive symptom. It’s a cramping, tired pain in the jaw muscles that builds while you chew and fades when you stop. It occurs in roughly 42% of biopsy-confirmed cases and is strongly predictive of the disease. Think of it like a leg cramp from walking, except it’s in your jaw from chewing.
Other common symptoms include:
- Low-grade fever and general fatigue or malaise
- Unintentional weight loss
- Morning stiffness in the shoulders or neck (especially when PMR is present)
- Visual disturbances such as double vision, blurriness, or brief episodes where vision goes dark in one eye
The Risk of Vision Loss
Vision loss is the most serious complication. In a study of 258 patients, about 34.5% experienced visual symptoms and 21.7% suffered permanent vision loss. The mechanism is straightforward: inflamed, narrowed arteries cut off blood supply to the optic nerve or retina, and the resulting damage can be irreversible within hours.
In nearly 29% of patients who lost vision, it happened suddenly with no preceding visual warning signs. Among those who did have earlier symptoms like flickering or brief blackouts, permanent loss followed within a median of 4.5 days. More than half of patients who lost vision did so before steroids were started, which is why treatment is typically begun immediately on clinical suspicion, before test results come back.
How It’s Diagnosed
Diagnosis relies on a combination of blood tests, imaging, and sometimes a tissue sample. The 2022 classification criteria from the American College of Rheumatology and EULAR use a points-based system. Age 50 or older is an absolute requirement. From there, different findings add points: a positive biopsy or ultrasound showing a characteristic “halo” around the temporal artery earns 5 points, while elevated inflammatory markers, sudden vision loss, or classic symptoms like jaw claudication and new headache each contribute additional points. A total score of 6 or more classifies the condition as GCA.
Blood Tests
Two standard blood markers help flag the condition. The erythrocyte sedimentation rate (ESR) measures how quickly red blood cells settle in a tube, which speeds up when inflammation is present. Normal ESR is under 22 for men and under 29 for women. In confirmed GCA, the median ESR is around 62. C-reactive protein (CRP), another inflammation marker, is normally under 8 but hits a median of 52 in active disease. Neither test is definitive on its own. Using optimal cutoffs (ESR above 53, CRP above 27), each catches roughly two-thirds to three-quarters of true cases but also flags some people who don’t have the disease.
Ultrasound and Biopsy
Ultrasound of the temporal arteries looks for a dark ring around the vessel wall, called the halo sign, which represents swelling. It’s a quick, noninvasive test with a median sensitivity of about 78% and specificity around 91%, meaning it’s good at ruling the disease in when positive but can miss some cases. Temporal artery biopsy, where a small segment of the artery is removed and examined under a microscope, has been the traditional gold standard. Its sensitivity is similar to ultrasound (median around 73%), and it can miss the disease when inflammation is patchy along the artery. In practice, many centers now use ultrasound as a first-line test and reserve biopsy for uncertain cases.
Treatment With Steroids
High-dose corticosteroids are the cornerstone of treatment, started as soon as the diagnosis is suspected. Most patients without vision loss begin oral steroids at roughly 1 to 1.5 mg per kilogram of body weight per day. For someone who has already lost vision, intravenous steroids at much higher doses are typically given for the first several days before switching to oral medication.
Steroids work fast. Headache and systemic symptoms often improve within days. The challenge is the taper: doses are gradually reduced over many months because dropping too quickly risks a flare. Most people remain on some level of steroid therapy for one to two years, and many experience side effects along the way, including weight gain, thinning bones, elevated blood sugar, and mood changes.
Steroid-Sparing Options
For patients who can’t tolerate long steroid courses or who keep flaring when doses are reduced, a biologic medication that blocks a specific inflammatory signal (interleukin-6) has become a major addition to treatment. In the landmark GiACTA trial, patients who received this medication achieved sustained remission at one year at rates 35% to 42% higher than those on steroids alone. Both weekly and every-other-week dosing schedules proved superior to standard steroid tapering. This allows many patients to reduce their total steroid exposure significantly, which matters for long-term bone health and metabolic side effects.
What Recovery Looks Like
Most people with temporal arteritis respond well to treatment and can eventually stop medication entirely, though the process takes patience. Relapses are common during the tapering phase, occurring in roughly half of patients. A relapse doesn’t mean treatment has failed. It usually means the dose was reduced a bit too quickly, and bumping it back up resolves symptoms. Regular blood work to track inflammation markers helps guide the taper.
Vision that was lost before or shortly after starting treatment rarely returns. However, once treatment is underway, the risk of further vision loss drops dramatically. The long game with temporal arteritis is managing the cumulative side effects of prolonged steroid use, which is why the steroid-sparing biologic option has changed the treatment landscape for patients who need it.