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High-resolution MRI for assessment of middle meningeal artery involvement in giant cell arteritis
  1. T A Bley1,2,
  2. J Geiger1,
  3. S Jacobsen3,
  4. O Wieben4,
  5. M Markl1,
  6. P Vaith5,
  7. T Grist2,
  8. M Langer1,
  9. M Uhl1
  1. 1
    Department of Diagnostic Radiology and Medical Physics, University Hospital Freiburg, Freiburg, Germany
  2. 2
    Department of Radiology, University of Wisconsin – Madison, Madison, Wisconsin, USA
  3. 3
    Department of Rheumatology, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark
  4. 4
    Department of Medical Physics, University of Wisconsin – Madison, Madison, Wisconsin, USA
  5. 5
    Department of Rheumatology and Clinical Immunology, University Hospital Freiburg, Freiburg, Germany
  1. T A Bley, University of Madison – Wisconsin, Department of Radiology, 600 Highland Avenue, Madison, Wisconsin 53792, USA; tbley{at}

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Giant cell arteritis (GCA) typically involves the superficial cranial arteries, the aorta and its branches. It has been discussed to which extent the vasculitic changes of the cranial arteries continue into the intracranial region. Autopsy findings have indicated that the characteristic signs of arteritic inflammation of GCA end after crossing the dural border.1 In a recent review of several published cases it was concluded that intracranial/intradural involvement in GCA is rare and represents a small subset of GCA that is non-responsive to corticosteroids and has a fatal course.2

Contrast-enhanced, high-resolution MRI allows non-invasive assessment of mural inflammation in the extracranial, superficial arteries in giant cell arteritis.3 Here, we report MRI findings suggestive of intracranial vasculitic involvement in patients with GCA. High-resolution MRI of 50 patients with GCA (15 men, 35 women, mean age 70.4 years) and signs of cranial arteritis in MRI scans acquired at 1.5 and 3 Tesla were retrospectively evaluated by 2 radiologists. Imaging parameters of the applied contrast enhanced, fat saturated multislice T1-weighted spin echo (SE) sequence have been reported elsewhere.4 5

Utilising the above-mentioned MRI protocol, mural thickening and contrast enhancement of the intracranial but extradural course of the medial meningeal artery (MMA), most likely representing mural inflammatory changes, was depicted in 16 patients (32%) (fig 1). These findings were bilateral in nine patients and unilateral in seven patients.

Figure 1

High-resolution T1-weighted contrast enhanced MRI of a 75-year-old woman with biopsy proven giant cell arteritis (GCA) readily reveals vasculitic changes of the superficial temporal artery (arrow in the enlarged image (D)). Note the central hypointense lumen due to flow void as compared to the homogeneously enhancing veins (arrowheads in (D)) where no flow void occurs due to slower venous flow. The medial meningeal artery presents with the same MRI signs of mural inflammation (arrow in (B)). High-resolution MRI with the same imaging settings as in (A), (B) and (D) in a 58-year-old woman with biopsy proven GCA reveal a medial meningeal artery without any MRI findings of mural inflammation (light arrow in enlargement (C)). The arteries of the circle of Willis (light arrows in (E)) and the basilar artery (light arrowhead in (D)) appear normal without any MRI signs of mural inflammation.

In 32 patients the diagnosis of GCA was established by positive temporal artery biopsy (TAB). In 6 of the other 18 patients TAB was negative. In these cases, as well as in the 12 cases in which no TAB was performed, GCA was established clinically by experienced rheumatologists utilising the American College of Rheumatology GCA 1990 criteria for classification.6

The thin walled intradural arteries of the circle of Willis did not present any signs on MRI suggestive of mural inflammation. This finding may not exclude intracranial, intradural involvement as the imaging parameters in this study were not optimised for assessment of the circle of Willis arteries. A prospective study with a dedicated MRI protocol for assessment of the intradural arteries could further address this issue.

Histological validation of MMA involvement is not feasible in vivo. However, leptomeningeal artery involvement in GCA has been found in various autopsy studies.7 8 The MRI findings reported here are highly suggestive of representing mural inflammatory changes of the MMA associated with GCA. They are similar to those seen in the superficial temporal artery in GCA, which have been validated by temporal artery biopsy in many cases.3

Positron emission tomography fails to visualise arteries of this calibre, especially with the overlaying uptake of the cerebral glucose metabolism. Colour-coded duplex ultrasonography has never been reported to depict mural inflammation of intracranial arteries in GCA. High-resolution MRI may be a valuable non-invasive imaging modality that can demonstrate characteristic signs of vascular inflammation in the intracranial arteries.


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  • Competing interests: None declared.

  • Ethics approval: Obtained.

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