3T MRI reveals extra- and intracranial involvement in giant cell arteritis

S Siemonsen1, C Brekenfeld2, B Holst2

  • 1From 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.

Abstract

Insights

Giant cell arteritis commonly shows inflammation in intracranial arteries, particularly the internal carotid artery (ICA). MR imaging can detect this mural inflammation, aiding in identifying affected patients.

Area of Science:

  • Neurology
  • Radiology
  • Vascular Medicine

Background:

  • Giant cell arteritis (GCA) is a systemic vasculitis affecting large and medium-sized arteries.
  • The extent of intracranial and intradural arterial involvement in GCA is not well-defined.

Purpose of the Study:

  • To prospectively evaluate the intracranial and intradural inflammatory vessel wall enhancement in patients with suspected GCA.
  • To assess mural changes in intracranial arteries using a specialized MR imaging protocol.

Main Methods:

  • 28 patients with suspected GCA underwent 3T MR imaging.
  • Imaging included fat-saturated T1WI pre- and postcontrast for intradural vessel wall enhancement and high-resolution imaging for extracranial vessels.
  • Vessel wall enhancement was independently assessed by two observers; temporal artery biopsies were available for 11 patients.

Main Results:

  • GCA was confirmed in 20 patients (9 biopsy-proven).
  • Intradural internal carotid artery (ICA) enhancement was detected in 10 patients; extracranial vessel enhancement in 16.
  • Slight vertebral artery enhancement was observed; vessel occlusion/stenosis correlated with enhancement sites in some cases.

Conclusions:

  • Intradural arterial wall enhancement, primarily in the ICA, is a common finding in GCA.
  • MR imaging detection of mural inflammation in the intradural ICA may identify a specific patient subgroup.
  • Further clinical studies are warranted to evaluate the significance of these findings.