Matthew J Thurtell1, Reid A Longmuir. 1. Departments of Ophthalmology and Visual Sciences (MJT, RAL) and Neurology (MJT), University of Iowa, Iowa City, Iowa Departments of Neurology (MJT) and Ophthalmology (RAL), VA Medical Center, Iowa City, Iowa.
Abstract
OBJECTIVE: Giant cell arteritis (GCA) is rarely reported as a cause of third nerve palsy. We describe the presentation and course of patients with third nerve palsy as the sole initial ocular manifestation of GCA. METHODS: Retrospective chart review of patients with third nerve palsy as the presenting sign of GCA. Symptoms, signs, and inflammatory marker levels at presentation and on follow-up were analyzed. All patients had imaging of the brain and circle of Willis, to exclude a compressive or inflammatory lesion, and had a temporal artery biopsy showing granulomatous arteritis. RESULTS: Four patients (aged 63-82) were identified and included. One patient had a complete third nerve palsy with pupil involvement, whereas the other 3 had third nerve palsies without pupil involvement. Three patients had ipsilateral periorbital/brow pain, and the other patient had temporal headache. Two patients reported no systemic symptoms of GCA but had elevated inflammatory markers. One patient had normal inflammatory markers but reported systemic symptoms of GCA. All patients had rapid improvement in symptoms and signs after high-dose oral prednisone was started with all showing complete recovery within weeks. CONCLUSIONS: GCA can rarely present with acute painful third nerve palsy, mimicking the presentation of a microvascular cause. The third nerve palsy often improves rapidly after steroid treatment is started. The presence of GCA symptoms or elevated inflammatory markers in a patient older than 50 years with an acute third nerve palsy should prompt initiation of high-dose steroid treatment and temporal artery biopsy.
OBJECTIVE:Giant cell arteritis (GCA) is rarely reported as a cause of third nerve palsy. We describe the presentation and course of patients with third nerve palsy as the sole initial ocular manifestation of GCA. METHODS: Retrospective chart review of patients with third nerve palsy as the presenting sign of GCA. Symptoms, signs, and inflammatory marker levels at presentation and on follow-up were analyzed. All patients had imaging of the brain and circle of Willis, to exclude a compressive or inflammatory lesion, and had a temporal artery biopsy showing granulomatous arteritis. RESULTS: Four patients (aged 63-82) were identified and included. One patient had a complete third nerve palsy with pupil involvement, whereas the other 3 had third nerve palsies without pupil involvement. Three patients had ipsilateral periorbital/brow pain, and the other patient had temporal headache. Two patients reported no systemic symptoms of GCA but had elevated inflammatory markers. One patient had normal inflammatory markers but reported systemic symptoms of GCA. All patients had rapid improvement in symptoms and signs after high-dose oral prednisone was started with all showing complete recovery within weeks. CONCLUSIONS: GCA can rarely present with acute painful third nerve palsy, mimicking the presentation of a microvascular cause. The third nerve palsy often improves rapidly after steroid treatment is started. The presence of GCA symptoms or elevated inflammatory markers in a patient older than 50 years with an acute third nerve palsy should prompt initiation of high-dose steroid treatment and temporal artery biopsy.