Learning Objectives
- •
Learn the common causes of headache.
- •
Learn the clinical presentation of temporal arteritis, including the unique symptom of jaw claudication.
- •
Learn how to use physical examination to identify physical findings associated with temporal arteritis.
- •
Learn to distinguish temporal arteritis from other pathologic processes that may mimic the disease.
- •
Learn the complications associated with temporal arteritis.
- •
Develop an understanding of the treatment options for temporal arteritis.
Hattie Harrison

“Doctor, I told Betty I was fine! Just a little headache. You know, everybody gets a headache now and then. I am just fine,” Hattie insisted. “I am a tough old bird.” I took her hand and looked her straight in the eye and said, “Hattie, I know you are tough, but Betty is really worried about you. She says that you are having trouble chewing your food and you’re losing weight. Let’s see what we can do to get you back on your feet!” She gave her daughter a defiant look and said, “I told you I am fine. Go take care of people that actually have something wrong with them!”
Hattie told me that her headache pain began about 2 weeks ago. She said that it just gradually came on. At first it was just an ache, but lately it is more severe. She said, “Doctor, it’s the craziest thing, but it hurts when I try to brush my hair.” Hattie went on to say that over the last week she found it hard to get comfortable because her head hurt all the time. Tylenol and aspirin helped a little, but she finally agreed to come in because her jaw had started hurting whenever she tried to chew her food. “Doctor, it’s kind of like a cramp in my jaw. If I try to keep chewing, the pain keeps getting stronger. If I rest for a minute, the cramping goes away, but if I try to chew again, the pain comes right back. It’s very strange!”
I asked Hattie what made her pain worse and she said, “Chewing.” I asked her what made the pain better, and she, without missing a beat, said, “Being left alone!” I laughed and asked if she had any problem going to the bathroom or was she losing any urine or feces or having any difficulty walking. Hattie shook her head adamantly from side to side. “Doctor, I can take care of myself.” And looking straight at Betty, she said, “Nobody is going to put me in the old folks, home!” I reassured her that she wasn’t going to the nursing home any time soon. I really didn’t know what Betty had on her mind, though, because Betty could be as stubborn as her mother. I told Hattie I was going to take a look at her and see what we could do to get her better.
On physical examination, Hattie was afebrile. Her eye exam revealed dense bilateral cataracts. I really couldn’t adequately visualize her optic discs. Her nose and throat examination, as well as her thyroid examination, were unremarkable. I asked Hattie if she was having any problem seeing or if anything had recently changed with her vision, and she snapped, “I can see better than you can!”
“Hattie, are you still driving?” I asked. Hattie glared at Betty and said, “Not since she took away my car keys!” “Mom,” Betty said, “you know I will take you wherever you want to go.” I made a note to refer Hattie to an ophthalmologist to look at her cataracts before she left the office.
Hattie’s cardiopulmonary examination revealed a grade 2 mitral valve systolic murmur, which I had noted on previous visits. Her abdominal examination was benign, with no abnormal mass or organomegaly. There was a trace of peripheral edema. Hattie’s radial pulses were 1+ bilaterally, but I was unable to identify any posterior tibial or dorsalis pedis pulses. What really concerned me was the finding of an inflamed, erythematous, thickened temporal artery on the left. The artery was easily visible and was so large that I could easily roll it between my fingers. A careful neurologic examination of the upper and lower extremities was unremarkable. No pathologic reflexes or clonus were identified.
Key Clinical Points—What’s Important and What’s Not
The History
- ◼
History of jaw claudication associated with headache
- ◼
No significant history of previous headache
- ◼
Difficulty eating due to persistent jaw claudication
- ◼
Denies any recent decrease in visual acuity
The Physical Examination
- ◼
Patient is afebrile
- ◼
Inflammation and thickening of the left temporal artery
- ◼
Dense cataract formation bilaterally
- ◼
No peripheral pulses in the lower extremities
- ◼
Normal neurologic examination
- ◼
No pathologic reflexes
- ◼
No clonus
Other Findings Of Note
- ◼
Grade 2 mitral valve murmur
What Tests Would You Like to Order?
- ◼
Urgent erythrocyte sedimentation rate (ESR)
- ◼
Urgent ultrasound and color Doppler image of the temporal arteries
- ◼
Urgent temporal artery biopsy
- ◼
Ultrasound of the aorta
Test Results
- ◼
ESR is 98.
- ◼
Ultrasound and color Doppler images of the temporal arteries reveal arterial luminal thickening and a positive halo sign, which is highly suggestive of temporal arteritis ( Figs. 11.1, 11.2 , and 11.3 ).
Fig. 11.1
Ultrasound of the left temporal artery with arterial wall thickening evident, consistent with temporal arteritis.
From Deyholos C, Sytek MC, Smith S, et al. Impact of temporal artery biopsy on clinical management of suspected giant cell arteritis. Ann Vasc Surg . 2020 [Fig. 1]. ISSN 0890-5096, https://doi.org/10.1016/j.avsg.2020.06.012 , http://www.sciencedirect.com/science/article/pii/S0890509620305136
Fig. 11.2
Transverse color Doppler image of the temporal artery demonstrating arterial luminal thickening and a positive halo sign, which is highly suggestive of temporal arteritis.
Fig. 11.3
Longitudinal color Doppler image in a patient with temporal arteritis demonstrating thickening of the wall of the temporal artery and a positive halo sign. Image is taken at the level just above the temporomandibular joint (TMJ) .
- ◼
Temporal artery biopsy reveals lymphoplasmacytic infiltrate associated with internal elastic lamina and medial destruction with marked intimal hyperplasia with resultant luminal obstruction consistent with severe temporal arteritis ( Fig. 11.4 ).
Fig. 11.4
Photomicrograph of temporal artery with lymphoplasmacytic infiltrate associated with internal elastic lamina and medial destruction with marked intimal hyperplasia with resultant luminal obstruction (Masson trichrome ×20).
From Pipinos II, Hopp R, Edwards WD, et al. Giant-cell temporal arteritis in a 17-year-old male. J Vasc Surg . 2006;43(5):1053–1055 [Fig. 2]. ISSN 0741-214, https://doi.org/10.1016/j.jvs.2005.12.043 , http://www.sciencedirect.com/science/article/pii/S0741521406000061
- ◼
Aortic ultrasound reveals thickening of the aortic wall with a large aortic dissection and associated false lumen and significant mural hematoma formation ( Fig. 11.5 ).
