ISSN 0017-8748 doi: 10.1111/head.12541 Published by Wiley Periodicals, Inc.
Headache © 2015 American Headache Society
Clinical Correspondence Magnetic Resonance Imaging of Temporal Arteritis: A Case Report Albi J. Chalissery, MBBS, MD; Timothy Barry, MB Bch BAO, MRCPI; Rosemary Lucey, MB Bch; Shakya Bhatacharjee, MRCPI; Peter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod); Eoin C. Kavanagh, FFR (RCSI); Brian Murray, MB Msc Key words: giant cell arteritis, temporal arteritis, magnetic resonance imaging, headache, temporal artery biopsy Abbreviations: GCA giant cell arteritis, MRI magnetic resonance imaging, TAB temporal artery biopsy (Headache 2015;55:866-868)
CASE A 75-year-old gentleman, nonsmoker with a history of hypertension and dyslipidemia, presented to the emergency department with a 6-week history of intermittent left-sided retromastoid headache and vertigo. He noted occasional pain in the jaw while chewing, and clinical examination revealed left post-auricular tenderness. Laboratory investigations showed an erythrocyte sedimentation rate (ESR) of 95 mm/hour and C reactive protein of 196 mg/L.Antinuclear antibody was weakly positive with a homogenous pattern. Considering the clinical symptoms and raised inflammatory markers, he was commenced on empirical high-dose corticosteroids for a presumptive diagnosis of giant cell arteritis. Given the history of
vertigo, magnetic resonance imaging (MRI) brain with diffusion-weighted imaging was performed to out rule a posterior circulation infarct or dissection. This demonstrated avid mural inflammation in the left temporal artery (Figs. 1 and 2) and occipital arteries. A left temporal artery biopsy (TAB) demonstrated chronic inflammation with giant cells and interruption of the internal elastic lamina (Fig. 3). After 2 days of highdose steroids, the patient’s symptoms had improved and ESR had reduced to 20 mm/hour. He was discharged on a tapering dose of steroids.
DISCUSSION Giant cell arteritis (GCA) affects large and medium-sized arteries, and involvement of superficial cranial vessels usually present with headache. The diagnosis of GCA (temporal arteritis) is based on the presence of at least 3 out of 5 features (age over 50 years, new headache, temporal artery tenderness or decreased pulsation on palpation, ESR greater than 50 mm per hour, and abnormal TAB) as per the
From the Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland (A.J. Chalissery, T. Barry, R. Lucey, S. Bhatacharjee, and B. Murray); Department of Pathology, Mater Misericordiae University Hospital, Dublin, Ireland (P. De La Harpe); Department of Neuroradiology, Mater Misericordiae University Hospital, Dublin, Ireland (E.C. Kavanagh). Address all correspondence to A.J. Chalissery, Eccles Street, Dublin 7, Dublin, Ireland.
Conflict of Interest: None.
Accepted for publication January 22, 2015.
No financial support towards this work received by any authors.
866
Headache
867
Fig 1.—MRI brain pre contrast T1 axial imaging of temporal artery on the left side.
Fig 2.—MRI brain post contrast T1 axial imaging of temporal artery on the left side showing avid enhancement and mural thickening of the artery.
American College of Rheumatology 1990 criteria.1 The gold standard for diagnosis is TAB showing vasculitis characterized by predominance of mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells. Various imaging modalities (color duplex ultrasonography, MRI, and 18F-fluorodeoxyglucose positron emission tomography) can aid the diagnosis of temporal arteritis by noninvasive means especially in biopsy negative cases.2-5 High-resolution MRI imaging studies can detect mural inflammation such as contrast enhancement of the vessel wall and of the perivascular spaces, and mural thickening in three major superficial cranial arteries (occipital artery, and frontal and parietal branches of the temporal artery).6 Although several cranial arteries could be affected simultaneously, the abnormalities are evident predominantly in the frontal branch. Involvement of occipital arteries with sparing of temporal arteries is also reported. Highresolution MRI examination was noted to have a
specificity and sensitivity of 0.80 for both in the detection of GCA diagnosis.3 In our case with biopsy proven temporal arteritis from frontal branch of the temporal artery on left side, we were able to
Fig 3.—Temporal artery biopsy showing disrupted elastic lamina (arrow) with infiltration of vessel wall (asterisk) with inflammatory cells including giant cells (circles).
868 demonstrate avid mural inflammation in the temporal artery and occipital artery on the ipsilateral side and occipital artery on the contralateral side. The current evidence shows that MRI could be used in detecting the patients with mural inflammation of the extra cranial arteries in GCA. This could guide the site of biopsy as the estimated false negative rate for TAB ranges from 7% to 61% due to segmental inflammation of the arteries.7 MRI could be considered as an additional noninvasive diagnostic modality in cases with negative TAB but fulfilling other features outlined by American College of Rheumatology 1990 criteria, but the signs of mural inflammation could rapidly reduce with duration of steroid treatment.
REFERENCES 1. Hunder GG, Bloch DA, Michel BA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. 1990;33:1122-1128.
June 2015 2. Schmidt WA. Role of ultrasound in the understanding and management of vasculitis. Ther Adv Musculoskelet Dis. 2014;6:39-47. 3. Siemonsen S, Brekenfeld C, Holst B, et al. 3T MRI reveals extra- and intracranial involvement in giant cell arteritis. Am J Neuroradiol. 2015;36:91-97. 4. Puppo C, Massollo M, Paparo F, et al. Giant cell arteritis: A systematic review of the qualitative and semiquantitative methods to assess vasculitis with 18F-fluorodeoxyglucose positron emission tomography. Biomed Res Int. 2014; doi:10.1155/2014/574248. 5. Prieto-Gonzalez S, Depetris M, Garcia-Martinez A, et al. Positron emission tomography assessment of large vessel inflammation in patients with newly diagnosed, biopsy-proven giant cell arteritis: A prospective, case-control study. Ann Rheum Dis. 2014; 73:1388-1392. 6. Bley TA, Weiben O, Uhl M, et al. Assessment of the cranial involvement pattern of giant cell arteritis with 3T magnetic resonance imaging. Arthritis Rheum. 2005;52:2470-2477. 7. Ashton-Key MR, Gallagher PJ. False-negative temporal artery biopsy. Am J Surg Pathol. 1992;16:634-635.
Headache © 2015 American Headache Society
Clinical Correspondence Magnetic Resonance Imaging of Temporal Arteritis: A Case Report Albi J. Chalissery, MBBS, MD; Timothy Barry, MB Bch BAO, MRCPI; Rosemary Lucey, MB Bch; Shakya Bhatacharjee, MRCPI; Peter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod); Eoin C. Kavanagh, FFR (RCSI); Brian Murray, MB Msc Key words: giant cell arteritis, temporal arteritis, magnetic resonance imaging, headache, temporal artery biopsy Abbreviations: GCA giant cell arteritis, MRI magnetic resonance imaging, TAB temporal artery biopsy (Headache 2015;55:866-868)
CASE A 75-year-old gentleman, nonsmoker with a history of hypertension and dyslipidemia, presented to the emergency department with a 6-week history of intermittent left-sided retromastoid headache and vertigo. He noted occasional pain in the jaw while chewing, and clinical examination revealed left post-auricular tenderness. Laboratory investigations showed an erythrocyte sedimentation rate (ESR) of 95 mm/hour and C reactive protein of 196 mg/L.Antinuclear antibody was weakly positive with a homogenous pattern. Considering the clinical symptoms and raised inflammatory markers, he was commenced on empirical high-dose corticosteroids for a presumptive diagnosis of giant cell arteritis. Given the history of
vertigo, magnetic resonance imaging (MRI) brain with diffusion-weighted imaging was performed to out rule a posterior circulation infarct or dissection. This demonstrated avid mural inflammation in the left temporal artery (Figs. 1 and 2) and occipital arteries. A left temporal artery biopsy (TAB) demonstrated chronic inflammation with giant cells and interruption of the internal elastic lamina (Fig. 3). After 2 days of highdose steroids, the patient’s symptoms had improved and ESR had reduced to 20 mm/hour. He was discharged on a tapering dose of steroids.
DISCUSSION Giant cell arteritis (GCA) affects large and medium-sized arteries, and involvement of superficial cranial vessels usually present with headache. The diagnosis of GCA (temporal arteritis) is based on the presence of at least 3 out of 5 features (age over 50 years, new headache, temporal artery tenderness or decreased pulsation on palpation, ESR greater than 50 mm per hour, and abnormal TAB) as per the
From the Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland (A.J. Chalissery, T. Barry, R. Lucey, S. Bhatacharjee, and B. Murray); Department of Pathology, Mater Misericordiae University Hospital, Dublin, Ireland (P. De La Harpe); Department of Neuroradiology, Mater Misericordiae University Hospital, Dublin, Ireland (E.C. Kavanagh). Address all correspondence to A.J. Chalissery, Eccles Street, Dublin 7, Dublin, Ireland.
Conflict of Interest: None.
Accepted for publication January 22, 2015.
No financial support towards this work received by any authors.
866
Headache
867
Fig 1.—MRI brain pre contrast T1 axial imaging of temporal artery on the left side.
Fig 2.—MRI brain post contrast T1 axial imaging of temporal artery on the left side showing avid enhancement and mural thickening of the artery.
American College of Rheumatology 1990 criteria.1 The gold standard for diagnosis is TAB showing vasculitis characterized by predominance of mononuclear cell infiltration or granulomatous inflammation, usually with multinucleated giant cells. Various imaging modalities (color duplex ultrasonography, MRI, and 18F-fluorodeoxyglucose positron emission tomography) can aid the diagnosis of temporal arteritis by noninvasive means especially in biopsy negative cases.2-5 High-resolution MRI imaging studies can detect mural inflammation such as contrast enhancement of the vessel wall and of the perivascular spaces, and mural thickening in three major superficial cranial arteries (occipital artery, and frontal and parietal branches of the temporal artery).6 Although several cranial arteries could be affected simultaneously, the abnormalities are evident predominantly in the frontal branch. Involvement of occipital arteries with sparing of temporal arteries is also reported. Highresolution MRI examination was noted to have a
specificity and sensitivity of 0.80 for both in the detection of GCA diagnosis.3 In our case with biopsy proven temporal arteritis from frontal branch of the temporal artery on left side, we were able to
Fig 3.—Temporal artery biopsy showing disrupted elastic lamina (arrow) with infiltration of vessel wall (asterisk) with inflammatory cells including giant cells (circles).
868 demonstrate avid mural inflammation in the temporal artery and occipital artery on the ipsilateral side and occipital artery on the contralateral side. The current evidence shows that MRI could be used in detecting the patients with mural inflammation of the extra cranial arteries in GCA. This could guide the site of biopsy as the estimated false negative rate for TAB ranges from 7% to 61% due to segmental inflammation of the arteries.7 MRI could be considered as an additional noninvasive diagnostic modality in cases with negative TAB but fulfilling other features outlined by American College of Rheumatology 1990 criteria, but the signs of mural inflammation could rapidly reduce with duration of steroid treatment.
REFERENCES 1. Hunder GG, Bloch DA, Michel BA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. 1990;33:1122-1128.
June 2015 2. Schmidt WA. Role of ultrasound in the understanding and management of vasculitis. Ther Adv Musculoskelet Dis. 2014;6:39-47. 3. Siemonsen S, Brekenfeld C, Holst B, et al. 3T MRI reveals extra- and intracranial involvement in giant cell arteritis. Am J Neuroradiol. 2015;36:91-97. 4. Puppo C, Massollo M, Paparo F, et al. Giant cell arteritis: A systematic review of the qualitative and semiquantitative methods to assess vasculitis with 18F-fluorodeoxyglucose positron emission tomography. Biomed Res Int. 2014; doi:10.1155/2014/574248. 5. Prieto-Gonzalez S, Depetris M, Garcia-Martinez A, et al. Positron emission tomography assessment of large vessel inflammation in patients with newly diagnosed, biopsy-proven giant cell arteritis: A prospective, case-control study. Ann Rheum Dis. 2014; 73:1388-1392. 6. Bley TA, Weiben O, Uhl M, et al. Assessment of the cranial involvement pattern of giant cell arteritis with 3T magnetic resonance imaging. Arthritis Rheum. 2005;52:2470-2477. 7. Ashton-Key MR, Gallagher PJ. False-negative temporal artery biopsy. Am J Surg Pathol. 1992;16:634-635.
