199. Comprehensive Assessment of Cranial and Orbital Vasculature on MRI in Patients with Giant Cell Arteritis

Background: Vessel wall MRI can depict changes consistent with arterial wall inflammation. Unlike temporal artery biopsy, MRI visualizes several full-length cranial arteries in a single scan mitigating the issue of sampling error. Furthermore, MRI evaluates orbital arteries posterior to the ocular globe, an area not visualized by ophthalmologic examination. While previous studies demonstrated good diagnostic performance of vessel wall MRI in evaluating temporal arteries in giant cell arteritis (GCA), little is known about changes to other cranial and orbital arteries. The goal of this study was to compare enhancement by MRI of multiple cranial and orbital arteries in patients with GCA versus controls.

Methods: Patients with suspected new or relapsing cranial GCA who underwent vessel wall brain and/or orbital MRI at presentation were included in the study. A clinical diagnosis of active ocular GCA or non-ocular GCA was determined by a rheumatologist and/or ophthalmologist and confirmed retrospectively. All MR images were scored by a single radiologist blinded to clinical data. Semi-quantitative integer scores of MRI enhancement were determined: scalp arteries were each scored 0, 1, 2, or 3 (score 2-3 defined as abnormal) and orbital structures were each scored 0, 1, or 2 (score 1-2 defined as abnormal). Differences in MRI findings between groups were determined using Fisher’s exact test.

Results: 30 patients had scalp arteries visualized on vessel wall MRI (final clinical diagnosis: 11 with GCA; 19 non-GCA) and 35 patients had orbital structures visualized on MRI (final clinical diagnosis: 4 ocular GCA; 9 non-ocular GCA; 22 non-GCA). No patient in the non-GCA group had abnormal scalp artery enhancement. Among patients diagnosed with GCA, temporal artery enhancement was the most common arterial abnormality (89%) followed by occipital artery enhancement (70%). One patient with GCA had isolated occipital artery enhancement without temporal artery involvement on MRI. Enhancement of the maxillary, facial, and external carotid arteries were seen in GCA but not in controls. In addition, MRI depicted multiple enhancing orbital structures which corresponded with vascular territories known to be affected by GCA; for example, optic nerve sheath and orbital intraconal fat enhancement were the most common findings on orbital MRI and corresponded to the anatomic location of the posterior ciliary arteries which are the main source of blood supply for the optic nerve (Figure 1C and 1D). No significant differences in orbital enhancement were observed between ocular and non-ocular GCA (all P > 0.05).

Conclusions : By comprehensively visualizing multiple cranial arterial territories, vessel wall MRI identified abnormal enhancement in arteries outside of the temporal arteries in patients with GCA vs controls. MRI enhancement was observed in orbital arteries known to be inflamed in ocular GCA. Interestingly, abnormal orbital enhancement was seen not only in clinically diagnosed ocular GCA patients (confirmed on fundoscopic exam) but also in a subset of patients without visual symptoms, suggesting that MRI may detect subclinical ocular disease in GCA. This study supports the possibility that vessel wall MRI may be a useful imaging tool that enhances current approaches to disease classification, risk stratification, and assessment of disease activity in GCA.

Disclosures: MAT – consultant for Horizon pharmaceuticals, UpToDate