Temporal Arteritis (Giant Cell Arteritis): Difference between revisions

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== Definition/Description  ==
== Introduction  ==
[[Image:Deep temporal arteries.png|500x300px|right|frameless]]Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref>&nbsp;
* The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the [[External Carotid Artery|carotid artery]].
* This condition is known as a condition of the elderly and is a significant cause of secondary [[headache]] in [[Older People - An Introduction|older adults]].
* GCA is closely linked to [[Polymyalgia Rheumatica|polymyalgia rheumatica]] (PMR), a systemic rheumatic inflammatory disorder with unknown causes<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>.
* GCA and PMR usually occur together in the same patient<ref name="chew" />.
[[Image:Deep temporal arteries.png|right|3x5px]]


Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.<ref name="chew"/>&nbsp;The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery. This condition is known as a condition of the elderly and is a significant cause of secondary headache in older adults. GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes<ref name="book">Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.</ref>. GCA and PMR usually occur together in the same patient<ref name="chew"/>.[[Image:Deep temporal arteries.png|left|500x300px]]
== Etiology ==
The exact etiology of GCA is currently unknown, various possibilities have been hypothesized
* Genetic,
* Environmental
* Autoimmune 
* An association with Toll-like receptor 4 gene polymorphism as well as HLA-DR4, has been identified<ref name=":0">Ameer MA, Peterfy RJ, Bansal P, Khazaeni B. Temporal (Giant Cell) Arteritis. StatPearls [Internet]. 2020 Jan.Available from: (last accessed 20.9.2020)https://www.ncbi.nlm.nih.gov/books/NBK459376/</ref>
* It is believed that the basis for the disease involves abnormalities of the arterial elasticum, with a decreased in integrity of the inner elastic membrane of affected arteries, resulting in a giant cell reaction near this elasticum.
* Another theory is that the initial lesion is a destruction of the muscular layers of the artery’s tunica media caused by ischemia, which leads to fragmentation of the elasticum with formation of giant cells occurring secondarily<ref name="gurwood" />.


[[Image:Deep temporal arteries.png|right|3x5px]]<br><br>
== Epidemiology  ==
 
* GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50<ref name="chew" /><ref name="sal">Salvarani C, Cantini F, Hunder G. Polymyalgia rheumatica and giant-cell arteritis. The Lancet. 2008;372(9634):234-245.</ref>.  
<br>
* 95% of cases occur in patients older than 55 years<ref name="K">Kawasaki A, Purvin V. Giant cell arteritis: an updated review. Acta Ophthalmologica. 2009;87(1):13-32.</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>.  
 
* The incidence of GCA in 70-79 year olds is 29.6 per 100,000 individuals<ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>. &nbsp;
 
* Women are 2-6 times more likely to be affected than men<ref name="chew" /><ref name="gurwood" /><ref name="wang">Wang X, Hu Z, Lu W, Tang X, Yang H, Zeng L et al. Giant cell arteritis. Rheumatol Int. 2008;29(1):1-7.</ref>.  
 
* Giant cell arteritis occurs in at least 25% of all cases of polymyalgia rheumatica (PMR)<ref name="book" />.  
 
* GCA is more frequent among people of Scandinavian and Northern European descent<ref name="chew" /><ref name="sal" />.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
== Prevalence<br>  ==
 
GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50<ref name="chew"/><ref name="sal">Salvarani C, Cantini F, Hunder G. Polymyalgia rheumatica and giant-cell arteritis. The Lancet. 2008;372(9634):234-245.</ref>. 95% of cases occur in patients older than 55 years<ref name="K">Kawasaki A, Purvin V. Giant cell arteritis: an updated review. Acta Ophthalmologica. 2009;87(1):13-32.</ref><ref name="gurwood">Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.</ref>. The incidence of GCA in 70-79 year olds is 29.6 per 100,000 individuals<ref name="smith">Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.</ref>. &nbsp;Women are 2-6 times more likely to be affected than men<ref name="chew"/><ref name="gurwood"/><ref name="wang">Wang X, Hu Z, Lu W, Tang X, Yang H, Zeng L et al. Giant cell arteritis. Rheumatol Int. 2008;29(1):1-7.</ref>. Giant cell arteritis occurs in at least 25% of all cases of polymyalgia rheumatica (PMR)<ref name="book"/>. GCA is more frequent among people of Scandinavian and Northern European descent<ref name="chew"/><ref name="sal"/>.<br><br>


== Characteristics/Clinical Presentation  ==
== Characteristics/Clinical Presentation  ==
[[Image:Symptoms-headache.jpg|right|400x300px]]The patient will usually present with complaints of a headache, painless vision loss, jaw claudication, fatigue, fever, anorexia, or temporal artery tenderness. 


Headaches/ generalized head pain, decreased visual acuity, diplopia, decreased color vision, visual field defect, aching/ stiffness of joints, conjunctival hyperanemia, cough, corneal oedema, iritis, cranial symptoms such as jaw claudication, temporal artery tenderness, amaurosis fugax, decreased temporal pulse, and scalp pain present in the majority of cases&nbsp;<ref name="book"/><ref name="sal"/><ref name="K"/><ref name="gurwood"/><ref name="smith"/>.
Patients may state that their headache has been occurring for a duration of 2 to 3 months and worsens with exposure to cold and at night when the pressure of the pillow causes pain to the artery. 
 
* On physical exam, the temporal artery may be thickened, painful, nodular, or erythema may occur on the overlying skin. 
<br><br>
* The temporal artery may not necessarily be the artery involved which further complicates the diagnosis. 
* Many patients will present with signs or symptoms of TIA or stroke. 
* The ophthalmologic exam will generally be benign, although if the circulation of the optic nerve is involved, the patient may display an afferent pupillary defect. 
* Because of the inconsistencies regarding the history and physical, temporal arteritis is often a difficult disease to diagnose in the emergency setting.<ref name=":0" />  


== Associated Co-morbidities  ==
== Associated Co-morbidities  ==


*Polymyalgia Rheumatica (PMR)  
*[[Polymyalgia Rheumatica]] (PMR)  
*Visual Disturbances  
*Visual Disturbances  
*Facial pain  
*Facial pain  
*Osteoporosis  
*[[Osteoporosis]]
*Hypokalemia  
*[[Hypokalemia]]
*Various infections such as oral/esophageal thrush  
*Various infections such as oral/esophageal thrush  
*Herpes Zoster<ref name="data">Petri H, Nevitt A, Sarsour K, Napalkov P, Collinson N. Incidence of Giant Cell Arteritis and Characteristics of Patients: Data-Driven Analysis of Comorbidities. Arthritis Care &amp; Research. 2015;67(3):390-395</ref><br><br>
*[[Herpes Zoster|Herpes Zoste]]<nowiki/>r<ref name="data">Petri H, Nevitt A, Sarsour K, Napalkov P, Collinson N. Incidence of Giant Cell Arteritis and Characteristics of Patients: Data-Driven Analysis of Comorbidities. Arthritis Care &amp; Research. 2015;67(3):390-395</ref>
 
== Medications  ==
 
High dose corticosteroids are the most widely accepted medication and overall treatment for GCA<ref name="chew"/><ref name="wang"/>. However, there is no consensus on dosage for either initial treatment or following rate of dosage reduction. Several entities such as the British Society for Rheumatology and the European League Against Rheumatism have developed guidelines on dosing based off extensive literature search<ref name="smith"/><ref name="schmidt">Schmidt J, Warrington K. Polymyalgia Rheumatica and Giant Cell Arteritis in Older Patients. Drugs &amp; Aging. 2011;28(8):651-666.</ref>- See "Medical Management" below.<br>
 
== Diagnostic Tests/Lab Tests/Lab Values  ==
 
GCA is diagnosed on the basis of the combination of&nbsp;symptoms, clinical findings, laboratory results, and&nbsp;diagnostic imaging<ref name="ness"/>.
 
*The gold standard diagnostic test for GCA is a temporal artery biopsy<ref name="K"/><ref name="gurwood"/><ref name="wang"/>.
*Increased ESR (erythrocyte sedimentation rate) &gt;50 mm/h is one of the five American College of Rheumatology criteria for the diagnosis of GCA<ref name="gurwood"/><ref name="smith"/><ref name="wang"/>.<br>


*CRP C-reactive protein is said to be increased in patients with GCA. It has been reported that CRP has a 100% sensitivity and when CRP is elevated in combination with ESR there is a 97% specificity<ref name="K"/><ref name="gurwood"/><ref name="wang"/>.
== Treatment  ==
*Thrombocytosis also serves as an important diagnostic tool for GCA. It has been shown that an elevated platelet may have a higher positive predictive value than ESR. In the setting of clinical suspicion and a raised ESR, thrombocytosis has a relatively high specificity for distinguishing GCA from other diseases<ref name="wang"/>.
*Plasma fibrinogen<ref name="gurwood"/>
*Newer diagnostic modalities, including ultrasound, magnetic resonance imaging, and positron emission tomography can play an important role in directing treatment in cases with negative TAB<ref name="K"/><ref name="smith"/>.<br>


<br> '''American College of Rheumatology classification criteria for giant cell arteritis- at least three of five must be met<ref name="chew"/><ref name="sal"/><ref name="wang"/>'''
The timing of treatment is critical in these patients to prevent vision loss. 
* Steroids should be started immediately upon suspicion of temporal arteritis. 
* Although there is no consensus among physicians regarding the amount of steroid therapy to begin, 60 milligrams of prednisone PO or 1 mg/kg daily can be used as a general guideline. This may be required for 1 to 2 years. 
* The patient should be followed by their primary care physician with frequent ESR draws. 
* If acute vision loss is present, the patient may be started on 250 mg to 1000 mg of intravenous (IV) steroids for 3 days. 
* Low-dose aspirin should also be started daily. 
* A rheumatologist should be consulted immediately upon starting steroid treatment and before performing a biopsy. 
* An ophthalmologist should also see the patient to perform a full eye exam to rule out other serious causes of vision loss<ref name=":0" />.<nowiki/>  


1.&nbsp;Age at onset 50 years or more<br>2. New-onset headache or localized headache<br>3. Tenderness or decreased pulsation in at least one of the temporal arteries<br>4. Erythrocyte sedimentation rate 50 mm/h or more<br>5. Abnormal artery biopsy with either mononuclear cell infiltrate or granulomatous inflammation (with giant cells)
== Evaluation  ==


'''<br>'''  
'''American College of Rheumatology classification criteria for giant cell arteritis- at least three of five must be met'''  


[[Image:Giant cell arteritis -- very low mag.jpg|right|300x200px]]
1.&nbsp;Age at onset 50 years or more<br>2. New-onset headache or localized headache<br>3. Tenderness or decreased pulsation in at least one of the temporal arteries<br>4. Erythrocyte sedimentation rate 50 mm/h or more<br>5. Abnormal artery biopsy with either mononuclear cell infiltrate or granulomatous inflammation (with giant cells)'''<ref name="chew" /><ref name="sal" /><ref name="wang" /><u></u>'''
== Physical Therapy Management  ==


== Etiology/Causes  ==
Physical Therapists should be aware of associated signs and symptoms and refer patients accordingly.
* Prompt initiation of treatment may prevent blindness and other ischemic related consequences.
* There are no current physical therapy treatment options for temporal arteritis and best management described in literature involves use of [[Corticosteroids in the Management of Rheumatoid Arthritis|corticosteroids]].&nbsp;
* The most important thing for physical therapists to be aware of are the clinical examination findings that are often associated with GCA. &nbsp;These include&nbsp;palpation&nbsp;of the temporal artery, auscultation of arteries&nbsp;including the subclavian and axillary, and bilateral&nbsp;[[Blood Pressure|blood pressure]] determination, looking for a&nbsp;predominant unilateral vascular stenosis<ref name="ness">Ness T, Bley TA, Schmidt WA, Lamprecht P. The diagnosis and treatment of giant cell arteritis. Dtsch Arztebl Int. 2013 May 23;110(21):376-86.</ref>


The overall etiology of GCA is unkown<ref name="sal"/>. &nbsp;Environmental factors are suspected to be potential triggers for this disease<ref name="chew"/><ref name="ness"/>.
== Prognosis ==
 
GCA is a systemic disease of variable presentation and duration.
It is believed that the basis for the disease involves abnormalities of the arterial elasticum, with a decreased in integrity of the inner elastic membrane of affected arteries, resulting in a giant cell reaction near this elasticum.
* In some patients, it has a course of a few years, while in others, the course is more chronic.  
 
* The majority of the patients taper and discontinue the steroids after a few years of the disease, but some may require long term administration.  
Another theory is that the initial lesion is a destruction of the muscular layers of the artery’s tunica media caused by ischemia, which leads to fragmentation of the elasticum with formation of giant cells occurring secondarily<ref name="gurwood"/>.<br>
* These patients are at risk of side effects of glucocorticosteroids and should be closely monitored.  
 
* GCA does not affect the overall survival rate of an individual except for those patients with aortitis and aortic dissection involvement<ref name=":0" />
== Systemic Involvement  ==
 
Less common symptoms affecting only about eight percent of those with the condition include: pleural effusion, coronary vasculitis, pericarditis, myocarditis, peripheral neuropathy, hearing loss, renal arteritis, lymph node hyperplasia, and abnormal liver function, mesenteric ischemia, sore throat, choking sensation.
 
Constitutional symptoms may include weight loss, malaise, fever, depression, and polymyalgia rheumatica, night sweats<ref name="chew">Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268</ref><ref name="gurwood"/><ref name="smith"/><ref name="ness"/><ref name="K"/>.<br>
 
== Medical Management (current best evidence)  ==
 
The goal of treatment is to minimize tissue damage caused by inadequate blood flow, and the most common route of management involves use of corticosteroids such as Prednisone. Below are dosage guidelines developed by the European League Against Rheumatism&nbsp;<ref name="chew" /><ref name="gurwood" /><ref name="smith" />.
 
'''<u>Initial steps:</u>'''
 
Prednisone 40 mg to 60 mg daily;<br>intravenous methylprednisolone<br>500 mg – 1 g × 3 days if visual<br>compromise or neurologic symptoms.<br>Treatment should not be withheld<br>pending TAB results.
 
'''<u></u>'''
 
<br>
 
'''<u>Next Steps:</u>'''
 
Gradual taper of prednisone by 10 mg
 
every 2 weeks to 20 mg, then 2.5 mg<br>every 2 weeks to 10 mg, then 1 mg<br>every month<ref name="smith"/>
 
== Physical Therapy Management (current best evidence)  ==
 
Physical Therapists should be aware of associated signs and symptoms and refer patients accordingly. Prompt initiation of treatment may prevent blindness and other ischemic related consequences.There are no current physical therapy treatment options for temporal arteritis and best management described in literature involves use of corticosteroids.&nbsp;<br>
 
The most important thing for physical therapists to be aware of are the clinical examination findings that are often associated with GCA. &nbsp;These include&nbsp;palpation&nbsp;of the temporal artery, auscultation of arteries&nbsp;including the subclavian and axillary, and bilateral&nbsp;blood pressure determination, looking for a&nbsp;predominant unilateral vascular stenosis<ref name="ness">Ness T, Bley TA, Schmidt WA, Lamprecht P. The diagnosis and treatment of giant cell arteritis. Dtsch Arztebl Int. 2013 May 23;110(21):376-86.</ref>
 
<br>  


== Differential Diagnosis  ==
== Differential Diagnosis  ==


*Central retinal artery occlusion[[Image:Symptoms-headache.jpg|right|400x300px]]
*Central retinal artery occlusion
*Acute glaucoma  
*Acute glaucoma
*Uveitic glaucoma  
*Uveitic glaucoma  
*Retrobulbar optic neuritis  
*Retrobulbar optic neuritis  
*Orbital abscess<br>
*Orbital abscess  
*Ophthalmic migraine  
*Ophthalmic migraine  
*Tolosa hunt syndrome  
*Tolosa hunt syndrome  
*Orbital and cavernous sinus compressive lesions  
*Orbital and cavernous sinus compressive lesions  
*Migraine headache  
*[[Migraine Headache|Migraine]] headache  
*Lyme disease  
*[[Lyme Disease|Lyme disease]]
*Herpes zoster ophthalmicus  
*Herpes zoster ophthalmicus  
*Trigeminal neuralgia  
*[[Trigeminal Neuralgia|Trigeminal neuralgia]]
*Diabetes  
*[[Diabetes]]
*Poorly Controlled hypertension  
*Poorly Controlled hypertension  
*Stress related disorders  
*[[Stress and Health|Stress]] related disorders  
*Angina pectoris&nbsp;<ref name="K"/><ref name="smith"/><br>
*[[Angina|Angina pectori]]<nowiki/>s&nbsp;<ref name="K" /><ref name="smith" />


== Case Reports/ Case Studies  ==
== Case Reports/ Case Studies  ==
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<br>  


<br>
== Recent Related Research (from [http://www.ncbi.nlm.nih.gov/pubmed/ Pubmed])  ==
<div class="researchbox">
<rss>http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1TUbR4JfRTvSrbbAM3hVX4olPV5UgCMCMh8k</rss>
</div>
== References  ==
== References  ==


<references /><br>  
<references /><br>  


[[Category:Bellarmine_Student_Project]]
[[Category:Bellarmine Student Project]]
[[Category:Autoimmune Disorders]]
[[Category:Rheumatology]]

Latest revision as of 21:42, 1 September 2023

 

Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Kiersten Young, Savannah Lane, Lucinda hampton, Elaine Lonnemann, 127.0.0.1, WikiSysop, Kim Jackson and Sehriban Ozmen  

Introduction[edit | edit source]

Deep temporal arteries.png

Temporal arteritis, also known as giant cell arteritis (GCA), is a systemic inflammatory vasculitis that affects medium-sized to large arteries.[1] 

  • The main arteries involved include the medium-sized muscular arteries, such as the cranial and extracranial branches of the carotid artery.
  • This condition is known as a condition of the elderly and is a significant cause of secondary headache in older adults.
  • GCA is closely linked to polymyalgia rheumatica (PMR), a systemic rheumatic inflammatory disorder with unknown causes[2].
  • GCA and PMR usually occur together in the same patient[1].
Deep temporal arteries.png

Etiology[edit | edit source]

The exact etiology of GCA is currently unknown, various possibilities have been hypothesized

  • Genetic,
  • Environmental
  • Autoimmune
  • An association with Toll-like receptor 4 gene polymorphism as well as HLA-DR4, has been identified[3]
  • It is believed that the basis for the disease involves abnormalities of the arterial elasticum, with a decreased in integrity of the inner elastic membrane of affected arteries, resulting in a giant cell reaction near this elasticum.
  • Another theory is that the initial lesion is a destruction of the muscular layers of the artery’s tunica media caused by ischemia, which leads to fragmentation of the elasticum with formation of giant cells occurring secondarily[4].

Epidemiology[edit | edit source]

  • GCA is the most frequent primary vasculitis, which predominantly affects Caucasian people over the age of 50[1][5].
  • 95% of cases occur in patients older than 55 years[6][4].
  • The incidence of GCA in 70-79 year olds is 29.6 per 100,000 individuals[7].  
  • Women are 2-6 times more likely to be affected than men[1][4][8].
  • Giant cell arteritis occurs in at least 25% of all cases of polymyalgia rheumatica (PMR)[2].
  • GCA is more frequent among people of Scandinavian and Northern European descent[1][5].

Characteristics/Clinical Presentation[edit | edit source]

Symptoms-headache.jpg

The patient will usually present with complaints of a headache, painless vision loss, jaw claudication, fatigue, fever, anorexia, or temporal artery tenderness.

Patients may state that their headache has been occurring for a duration of 2 to 3 months and worsens with exposure to cold and at night when the pressure of the pillow causes pain to the artery.

  • On physical exam, the temporal artery may be thickened, painful, nodular, or erythema may occur on the overlying skin.
  • The temporal artery may not necessarily be the artery involved which further complicates the diagnosis.
  • Many patients will present with signs or symptoms of TIA or stroke.
  • The ophthalmologic exam will generally be benign, although if the circulation of the optic nerve is involved, the patient may display an afferent pupillary defect.
  • Because of the inconsistencies regarding the history and physical, temporal arteritis is often a difficult disease to diagnose in the emergency setting.[3]

Associated Co-morbidities[edit | edit source]

Treatment[edit | edit source]

The timing of treatment is critical in these patients to prevent vision loss.

  • Steroids should be started immediately upon suspicion of temporal arteritis.
  • Although there is no consensus among physicians regarding the amount of steroid therapy to begin, 60 milligrams of prednisone PO or 1 mg/kg daily can be used as a general guideline. This may be required for 1 to 2 years.
  • The patient should be followed by their primary care physician with frequent ESR draws.
  • If acute vision loss is present, the patient may be started on 250 mg to 1000 mg of intravenous (IV) steroids for 3 days.
  • Low-dose aspirin should also be started daily.
  • A rheumatologist should be consulted immediately upon starting steroid treatment and before performing a biopsy.
  • An ophthalmologist should also see the patient to perform a full eye exam to rule out other serious causes of vision loss[3].

Evaluation[edit | edit source]

American College of Rheumatology classification criteria for giant cell arteritis- at least three of five must be met

1. Age at onset 50 years or more
2. New-onset headache or localized headache
3. Tenderness or decreased pulsation in at least one of the temporal arteries
4. Erythrocyte sedimentation rate 50 mm/h or more
5. Abnormal artery biopsy with either mononuclear cell infiltrate or granulomatous inflammation (with giant cells)[1][5][8]

Physical Therapy Management[edit | edit source]

Physical Therapists should be aware of associated signs and symptoms and refer patients accordingly.

  • Prompt initiation of treatment may prevent blindness and other ischemic related consequences.
  • There are no current physical therapy treatment options for temporal arteritis and best management described in literature involves use of corticosteroids. 
  • The most important thing for physical therapists to be aware of are the clinical examination findings that are often associated with GCA.  These include palpation of the temporal artery, auscultation of arteries including the subclavian and axillary, and bilateral blood pressure determination, looking for a predominant unilateral vascular stenosis[10]

Prognosis[edit | edit source]

GCA is a systemic disease of variable presentation and duration.

  • In some patients, it has a course of a few years, while in others, the course is more chronic.
  • The majority of the patients taper and discontinue the steroids after a few years of the disease, but some may require long term administration.
  • These patients are at risk of side effects of glucocorticosteroids and should be closely monitored.
  • GCA does not affect the overall survival rate of an individual except for those patients with aortitis and aortic dissection involvement[3]

Differential Diagnosis[edit | edit source]

Case Reports/ Case Studies[edit | edit source]

1. Colin G, Dupont M. Giant cell arteritis. Journal of the Belgian Society of Radiology. 2013;96(5):290.

http://br.ubiquitypress.com/articles/10.5334/jbr-btr.406/galley/403/download/


2. Lockhart M, Robbin M. Case 58: Giant Cell Arteritis1. Radiology. 2003;227(2):512-515.

http://pubs.rsna.org/doi/pdf/10.1148/radiol.2272010487


3. De Hertogh W, Vaes P, Versijpt J. Diagnostic work-up of an elderly patient with unilateral head and neck pain. A case report. Manual Therapy. 2013;18(6):598-601.

https://www.researchgate.net/profile/Willem_De_Hertogh/publication/232086111_Diagnostic_work-up_of_an_elderly_patient_with_unilateral_head_and_neck_pain_A_case_report/links/0deec527d1346ac25a000000.pdf


References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Chew S, Kerr N, Danesh-Meyer H. Giant cell arteritis. Journal of Clinical Neuroscience. 2009;16(10):1263-1268
  2. ↑ 2.0 2.1 Goodman C, Snyder T. Differential diagnosis for physical therapists. St. Louis, Mo.: Saunders/Elsevier; 2013.
  3. ↑ 3.0 3.1 3.2 3.3 Ameer MA, Peterfy RJ, Bansal P, Khazaeni B. Temporal (Giant Cell) Arteritis. StatPearls [Internet]. 2020 Jan.Available from: (last accessed 20.9.2020)https://www.ncbi.nlm.nih.gov/books/NBK459376/
  4. ↑ 4.0 4.1 4.2 Gurwood A, Malloy K. Giant cell arteritis. Clinical and Experimental Optometry. 2002;85(1):19-26.
  5. ↑ 5.0 5.1 5.2 Salvarani C, Cantini F, Hunder G. Polymyalgia rheumatica and giant-cell arteritis. The Lancet. 2008;372(9634):234-245.
  6. ↑ 6.0 6.1 Kawasaki A, Purvin V. Giant cell arteritis: an updated review. Acta Ophthalmologica. 2009;87(1):13-32.
  7. ↑ 7.0 7.1 Smith J, Swanson J. Giant Cell Arteritis. Headache: The Journal of Head and Face Pain. 2014;54(8):1273-1289.
  8. ↑ 8.0 8.1 Wang X, Hu Z, Lu W, Tang X, Yang H, Zeng L et al. Giant cell arteritis. Rheumatol Int. 2008;29(1):1-7.
  9. ↑ Petri H, Nevitt A, Sarsour K, Napalkov P, Collinson N. Incidence of Giant Cell Arteritis and Characteristics of Patients: Data-Driven Analysis of Comorbidities. Arthritis Care & Research. 2015;67(3):390-395
  10. ↑ Ness T, Bley TA, Schmidt WA, Lamprecht P. The diagnosis and treatment of giant cell arteritis. Dtsch Arztebl Int. 2013 May 23;110(21):376-86.


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