Can headache caused by temporal arteritis be relieved by NSAIDS and analgesics? How long does an episode last? How can someone differentiate between temporal arteritis associated headache and other types of headaches?
Temporal arteritis is a condition that causes inflammation of arteries— the blood vessels that carry oxygen-rich blood from the heart. The exact cause of temporal arteritis is unknown, but the inflammation appears to be a result of the immune
system overreacting and attacking the body’s own tissues. It is more common
among older patients, and almost never occurs under the age of 55. The “temporal artery” is the name of a specific artery located on each side of the head. In the
condition known as temporal arteritis, there is inflammation of numerous blood vessels, but the temporal arteries are almost always affected. Inflammation of arteries causes reduced blood flow, which is why this disease can cause severe
symptoms.
Treatment
It is common for patients with temporal arteritis to require pred-nisone for a year or more. Relatively high doses are typically required until the symptoms have resolved and the vision has become stable. Blood tests are repeated frequently to make sure it is safe to slowly lower the dose of the medications. If high doses of prednisone cause intolerable side effects, then other medications can be used to help lower the dose of prednisone. These include other medications that suppress the immune system such as aza-thioprine (Imuran) and mycophenilate mofetil (Cell Cept).
Steroids:Once the diagnosis is suspected, treat with high-dose corticosteroid immediately:[3]
40 mg prednisolone daily unless the patient has ischaemic symptoms (jaw or tongue claudication, or visual symptoms).
Claudication symptoms: give 60 mg prednisolone daily.
If the patient has visual symptoms, admit for treatment with intravenous methylprednisolone.
Once symptoms and abnormal test results resolve, the dose can be reduced in 10 mg steps each two weeks to 20 mg, then in 2.5 mg steps.
Flare-ups and relapses usually respond to corticosteroid increases to the level at which symptoms previously were controlled. Protracted courses of therapy are often necessary.[8]
Low-dose aspirin:[9]Start aspirin 75 mg daily unless there are contra-indications - eg, active peptic ulceration or a bleeding disorder.
Start gastroprotection with a proton pump inhibitor in view of added risk of peptic ulceration with high-dose steroids and aspirin.
Low-dose aspirin has been shown to decrease the rate of visual loss and strokes in patients with GCA.[10]
Other treatments: although steroids remain the cornerstone of therapy for GCA, patients with long-standing, recalcitrant disease may be considered for treatment with methotrexate, azathioprine or tumour necrosis factor-alpha inhibitors.[11]
In addition to Rafik's comments, I have a few more points to add.
Accurate diagnosis is essential - temporal artery biopsy and/or ultrasound are the best methods to confirm the diagnosis, but should be performed without delay
There is evidence that Tocilizumab (anti-IL6) may be useful for patients who have contraindications to steroids or relapse on steroids
Bone protection with bisphosphonates advisable.
Watch out for those with a prior history of diverticular disease as they are prone to perforation on high dose steroids.
In my opinion, follow up should normally be supervised by a rheumatologist. I hope this helps
Your specific questions about headaches and TA were really not answered by your two correspondents who gave you more or less irrelevant general textbook materials. I would invite them to share their clinical reasoning and expert experience in answering the questions.
1-NSAIDS: aspirin with a dose of 75 mg is used (as indicated in my first answer).
2-TA headache cycle: I have not found any data on how much time the headache attack lasts in each cycle. From my experience there is no fixed value; it varies from person to person.
Since you have stated that we have answered the question based on information from textbooks and not based on clinical experience, it is the best time that you give us our first lesson on how to address clinical questions. The first lesson will be answering the specific questions of Alia.
I suggest that you cool down and NOT attack the answers of persons that you do not know their educational background.
In 1981, I have earned my pharmacy degree and since I practice pharmacy and see around 100 patients/day. I know exactly what I am talk about; it is a mixture of experience and textbooks.
Hoping next time your answers will NOT be aggressive.
My interventions were intended to have people come up with specific answers to Alia's legitimate clinical questions (which, as is, are not easy to answer because they need to be rephrased and contextualized). The fact is that neither she nor I, found answers in the contributions that were first posted. I am glad that you did share your experience, this second time around. My intervention was thus not aggressive nor insulting as you perceived it. Just matter-of-factly!
As a student, Alia's role is to read what's in the book and all students are expected to do so before asking a question on this site. As mentors/experts, our role is to teach her what is not in the books and share in the discussion. That is how I understand the use of ResearchGate.net. Why don't Alia give us her tentative short answers to her questions:
Q1. How long does TA-related headache last?
NB. I removed the word "episode" which is misleading in that situation.
Q2. Does it respond to OTC NSAIDs/analgesics?
Q3. How to differentiate TA-related vs non-related headache?
I will jump in after with my own answers.
on this note, my wife calls me for dinner. Looking forward to our next epistolary meeting. Best wishes
Henri A. Ménard MD FRCP(C), Emeritus Professor of Medicine, McGill University
I would like to thank you all for your answers. I am honored to have people of great scientific background participate in answering my question. I have gained helpful things from each and every answer. I am really thankful to you all.
1. Trested PMR/TA has a natural history of 1-2 yrs. The typical headaches shoud disappear in the first 1-2 months on Pred and with adequate dosing, they should not recur. The clinical difficulty is how to interpret recurring symptoms after 5-6 months during prednisone tapering. Those are a mixture of mild inflammatory C-spine/shoulder on OA in an elderly polysymptomatic person. Normal acute phase reactants are reassuring but a mild elevation, is problematic as it can be non specific. Trial of NSAIDs (before Pred) are useful and may be enough.
2. NSAIDs are not the primary trestment but can be useful empirically later in recurring PMR-like atypical symptoms.
3. The typical headaches at onset are easy to identify. The 18-month-recurring headaches are more difficult (vide supra) and it becomes the art of personlized medicine to deal with them according to the « primo non nocere » principle.