Temporal artery enhancement on cranial magnetic resonance imaging

A 68-year-old white female presented to her outside ophthalmologist with acute vision loss in the left eye (OS) described as a “green line across the top half of her vision” and dull pain OS. She then experienced progressive worsening of vision OS, pain with chewing, temple pain, and scalp tenderness. The visual acuity was 20/20 in the right eye (OD) and counting fingers at 1/2-foot distance OS. There was a left relative afferent pupillary defect and optic disc edema OS. The right optic nerve was normal, but the cup-to-disc ratio was 0.4 OD. The remainder of the eye examination was normal OU. An erythrocyte sedimentation rate (ESR) was 25 mm/h, a C-reactive protein (CRP) level was <0.30 mg/dL, and platelet count was 349 × 10³/mm³. She was started on oral prednisone 60 mg/day. Medical history was significant for hypertension and Raynaud phenomenon. The remainder of the social, family, allergy, and medication history was noncontributory. She denied the use of any immunosuppressive drugs. The patient was then referred to the neuro-ophthalmology service at Houston Methodist Hospital. Cranial magnetic resonance imaging (MRI) with and without contrast for atypical headache and amaurosis fugax at the outside facility showed on the T1 precontrast axial MRI some mural thickening of the left superficial temporal artery. T1-weighted, fat-suppressed, postcontrast axial MRI showed mural enhancement of the artery and a partial flow void on all sequences consistent with partial arterial flow in the vessel more consistent with an artery rather than a vein (Fig. 1). Axial T2 MRI demonstrated the course of the superficial temporal artery all the way down to the internal maxillary artery (Fig. 2).

A left-sided temporal artery biopsy (TAB) taken at the same anatomical site as the enhancing artery seen radiographically on the MRI was positive for giant cell arteritis (GCA). Additional special staining with Movat pentachrome stain showed disruption of the internal elastic lamina, and additional immunohistochemistry studies using CD68 were positive for macrophages consistent with the diagnosis of GCA. Three months after the positive TAB, the patient reported recurrence of temple headache and scalp tenderness. ESR and CRP results were normal. She underwent repeat cranial MRI at the outside facility. Comparison of the pre- and post-TAB cranial MRI with gadolinium showed postoperative reduction in the size of the previously enhancing temporal artery, and there was some residual surrounding soft-tissue edema caused by postoperative changes at the site of the left TAB (Fig. 3, Fig. 4).

GCA is a chronic vasculitis of elderly adults that manifests in large- and medium-sized arteries.^,  The diagnosis is a clinical one supported by elevated acute-phase reactants (e.g., ESR and CRP) and confirmed histologically by a TAB. Cranial and orbital MRI studies are generally not performed and are usually not necessary for the diagnosis of GCA, but a few prior MRI studies have demonstrated similar radiographic findings in the temporal artery in GCA. We suspect that these MRI findings may be underrecognized in GCA. Bley et al.^,  reported the use of high-resolution MRI in revealing mural inflammatory changes of the temporal artery in GCA. Similar findings have been seen with variable sensitivity and specificity by ultrasound of the temporal artery but have not superseded the use of the presumed gold standard of the TAB. Nevertheless, the presence of these MRI findings might prompt a clinician evaluating an elderly patient to more aggressively evaluate and treat for GCA.

Although clinical suspicion, elevated serum acute-phase reactants, and a positive TAB are critical for the diagnosis of GCA, we believe that these MRI findings suggestive of GCA occasionally might be useful to clinicians, especially for elderly patients who have already undergone neuroimaging for headache or other nonspecific complaints of GCA.