Giant cell arteritis and mri findings

On average, the cortisone therapy began 3 days 9 hr. A biopsy of the temporal artery was performed for 16 of the 20 patients after the MRI examination as the most reliable way to diagnose GCA.

Biopsy specimens were taken from the same frontal branch of the superficial temporal artery as that imaged with MRI. Clinical and laboratory signs of GCA were reevaluated when the patients were receiving corticosteroid medication. View larger version 60K Fig. No or slight enhancement is considered physiologically normal, whereas prominent or strong mural enhancement indicates mural inflammation. Nitroglycerine capsule used as fiducial marker appears as white ball in A and C.

No enhancement year-old woman. View larger version 65K Fig. Slight enhancement year-old man. View larger version 73K Fig. Prominent enhancement year-old man. View larger version 68K Fig. Strong enhancement year-old man. The images of all patients had good diagnostic quality, and the temporal artery was clearly depicted.

The lumen of the temporal veins was bright on enhanced scans, whereas the lumen of the temporal artery showed low signal intensity because of the so-called flow-void phenomenon. This is caused by the inflow of faster-moving spins in the arteries and helps to differentiate temporal arteries from temporal veins, as depicted in Figures 2A and 2B. View larger version K Fig.

Diagnosis and extension of giant cell arteritis. Contribution of imaging techniques - EM|consulte

View larger version 87K Fig. Contrast-enhanced, fat-saturated T1-weighted 2D spin-echo sequence at same position as A shows bright contrast enhancement of thickened vessel wall, strongly indicating arteritis arrow. Concomitant bright signal intensity of lumen of temporal vein arrowheads and low signal intensity of lumen of temporal artery are due to flow-void phenomenon arrow.

The average wall thickness of the inflamed arteries was 0. The mean value for C-reactive protein was The headache symptoms decreased in all 17 GCA-positive patients after treatment with corticosteroids. Biopsy samples were taken from 15 of these patients and showed 13 to have had true-positive findings and two, false-negative findings.

Table 2 summarizes the data from the other 3 patients, in whom GCA had been suspected but was excluded on the basis of their clinical course and the ACR criteria. The average wall thickness of the arteries was 0. The mean value for C-reactive protein was 5. This study demonstrated the feasibility of using high-resolution MRI to visualize mural inflammatory changes, even in small arteries.


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Compared with the diagnosis obtained using the ACR criteria, diagnosis using MRI was true-positive in 16 patients and true-negative in 3 patients. The only patient whose MRI findings were false-negative also had false-negative histologic findings. It is possible that an unaffected artery was examined at histology and MRI, or GCA might have occurred in vessels outside the field of view of MRI, such as in the occipital arteries. The measurements of the vessel wall and lumen, both inflamed and unaffected, correlated closely to those reported by Schmidt et al.

They found average values for the wall thickness of the frontal branch of the superficial frontal artery of 0. Mural contrast enhancement on MRI is a well-recognized sign of acute inflammatory changes [ 12 , 13 ]. Typically, enhancement persists long after the contrast agent has left the vascular system [ 13 ]. Therefore, long T1-weighted sequences of up to 6 min can be used to acquire images with high spatial resolution and sufficient signal-to-noise ratio, as we demonstrated here. The unenhanced images without fat suppression added helpful anatomic information.

However, they were not used for the diagnosis and might be omitted in future protocols to reduce total imaging time. Inflammation of the temporal artery has been shown to have a segmental distribution [ 14 , 15 ]. This may be a reason for false-negative results from biopsies. High-resolution MRI may be used to localize segments with the most intense mural inflammatory changes to determine the best site for biopsy.

Potentially, such localization may reduce the number of biopsy specimens falsely negative for inflammation. Achkar et al. Nevertheless, we tried to image the temporal artery as early as possible after initial clinical presentation. For monitoring the activity of inflammation under long-term corticosteroid therapy, repeated biopsy of the temporal artery was recommended by Harbison and colleagues [ 17 ].

Eventually, high-resolution MRI of the temporal artery may be used instead of repeated biopsies to monitor mural inflammatory changes under therapy. Recognizing that negative biopsy findings for the temporal artery cannot exclude GCA [ 15 ], we used two reference standards: findings of the biopsy alone and clinical criteria as proposed by the ACR. Therefore, we are convinced that GCA was the correct diagnosis in those patients.

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However, our study also had some limitations: First, because this was our initial experience with MRI of GCA, we collected data from only a few patients. Therefore, we did not assess the sensitivity and specificity of the method. Trials using more patients are warranted for statistical purposes and are under way. Second, all patients were referred to us with clinically suspected GCA, and this referral cohort may have led to a referral bias.

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Nevertheless, the bright contrast enhancement seen in our patients remains a strong sign of mural inflammation. Youngstein, T. Fendler, W. J Nucl Med 57 , — Yoo, H. Korean J Radiol 16 , 32—49 Czernin, J. Literature Evidence from More Than Patients. J Nucl Med 55 , 59S—62S Einspieler, I. Clin Radiol Ishikawa, K. J Am Coll Cardiol 12 , — Sharma, B. Diagnostic criteria for Takayasu arteritis. Int J Cardiol 54 Suppl , S— Hunder, G.

The American College of Rheumatology criteria for the classification of giant cell arteritis. Arthritis Rheum 33 , — Slart, R. Desai, M.


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Diagnostic Value of High-Resolution MR Imaging in Giant Cell Arteritis

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Computed Tomography

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