S Siemonsen1, C Brekenfeld2, B Holst2, A-K Kaufmann-Buehler2, J Fiehler2, T A Bley3. 1. From the Department of Diagnostic and Interventional Neuroradiology (S.S., T.A.B.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany s.siemonsen@uke.uni-hamburg.de. 2. Department of Diagnostic and Interventional Radiology (C.B., B.H., A.-K.K.-B., J.F.), University Hospital of Würzburg, Würzburg, Germany. 3. From the Department of Diagnostic and Interventional Neuroradiology (S.S., T.A.B.), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Abstract
BACKGROUND AND PURPOSE: The frequency and amount of intracranial, intradural inflammatory vessel wall enhancement in giant cell arteritis remain unclear. The purpose of this work was to prospectively assess the intracranial extent of vasculitic changes in patients with giant cell arteritis using a dedicated MR imaging protocol optimized for assessment of mural changes of intracranial arteries. MATERIALS AND METHODS: Twenty-eight patients with suspected giant cell arteritis underwent 3T MR imaging. Imaging included a fat-saturated T1WI pre- and postcontrast application optimized for assessment of intradural vessel wall enhancement and high-resolution fat-saturated T1WI to evaluate superficial extracranial vessels. Temporal artery biopsies were available in 11 cases. Vessel wall enhancement of intradural and extracranial vessels was evaluated by 2 observers independently. RESULTS: Twenty patients had giant cell arteritis; 9 cases were biopsy-proved. Clear vessel wall enhancement of superficial extracranial and intradural internal carotid arteries was detected in 16 and 10 patients, respectively. Slight vessel wall enhancement of the vertebral arteries was seen. Of 9 patients with giant cell arteritis with vessel occlusion or stenosis, 2 presented with cerebral ischemic infarcts. Vessel occlusion or stenosis site coincided with the location of vessel wall enhancement of the vertebral arteries in 4 patients and of the intradural ICA in 1 patient. CONCLUSIONS: Vessel wall enhancement of intradural arteries, mainly the ICA, can be regularly found in patients with giant cell arteritis. Mural inflammatory changes of the intradural ICA detected on MR imaging may identify a subgroup of patients with giant cell arteritis and should be further evaluated in clinical studies.
BACKGROUND AND PURPOSE: The frequency and amount of intracranial, intradural inflammatory vessel wall enhancement in giant cell arteritis remain unclear. The purpose of this work was to prospectively assess the intracranial extent of vasculitic changes in patients with giant cell arteritis using a dedicated MR imaging protocol optimized for assessment of mural changes of intracranial arteries. MATERIALS AND METHODS: Twenty-eight patients with suspected giant cell arteritis underwent 3T MR imaging. Imaging included a fat-saturated T1WI pre- and postcontrast application optimized for assessment of intradural vessel wall enhancement and high-resolution fat-saturated T1WI to evaluate superficial extracranial vessels. Temporal artery biopsies were available in 11 cases. Vessel wall enhancement of intradural and extracranial vessels was evaluated by 2 observers independently. RESULTS: Twenty patients had giant cell arteritis; 9 cases were biopsy-proved. Clear vessel wall enhancement of superficial extracranial and intradural internal carotid arteries was detected in 16 and 10 patients, respectively. Slight vessel wall enhancement of the vertebral arteries was seen. Of 9 patients with giant cell arteritis with vessel occlusion or stenosis, 2 presented with cerebral ischemic infarcts. Vessel occlusion or stenosis site coincided with the location of vessel wall enhancement of the vertebral arteries in 4 patients and of the intradural ICA in 1 patient. CONCLUSIONS: Vessel wall enhancement of intradural arteries, mainly the ICA, can be regularly found in patients with giant cell arteritis. Mural inflammatory changes of the intradural ICA detected on MR imaging may identify a subgroup of patients with giant cell arteritis and should be further evaluated in clinical studies.
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