Letters to the Editor
We report for the first time the concurrence of ischemic optic neuropathy and third cranial nerve palsy in a case of histologically proven giant cell arteritis (GCA).
An 87-year-old woman was admitted to the hospital with a 4-week history of pain on her scalp, under her chin, and in the occipital area and neck. In addition, she had jaw claudication, which gradually increased in intensity. One day earlier, the patient simultaneously developed sudden profound vision loss and ptosis of the right eye. She had lost the vision in the left eye many years earlier from direct trauma.
Our examination revealed a best-corrected visual acuity of 20/200 in the right eye and no light perception in the left eye. The right pupil measured 5 mm in dim illumination and did not constrict to direct light. The left pupil was irregular, measured about 2.5 mm, and did not constrict to direct light. The right upper lid had 3 mm of ptosis. In the right eye, abduction was normal, but adduction, supraduction, and infraduction were absent. Ophthalmoscopy of the right eye revealed mild optic disc swelling. Evaluation of the left eye could not be done because of the history of trauma. Pulsations of the right temporal artery were not palpable, and those of the left temporal artery were feeble. There was scalp tenderness.
The erythrocyte sedimentation rate was 55 mm/h (normal value <15 mm/h), C-reactive protein (CRP) was 8.3 mg/L (normal value <6 mg/L), and platelet count was 625,000/μL (normal value 142,000-424,000/μL). Brain MRI was normal. On color duplex ultrasonography, no fluximetric alterations of carotid and vertebral arteries were seen.
The following day, biopsy of the right temporal artery showed marked inflammation and intimal fibrosis (Fig. 1). The media contained lymphocytes and giant cells. Fragmentation of the internal elastic lamina of the artery was evident. A diagnosis of giant cell arteritis was made and treatment with 50 mg oral prednisolone was started. Within a few days, the headache disappeared. The medication was continued at the same dose for 20 days, after which the dose was tapered. Three months after the corticosteroid treatment was started, the features of third cranial nerve palsy had disappeared except for a dilated unreactive pupil. The vision loss persisted.
Impairment of the third, fourth, or sixth cranial nerves has been reported in only 2% of patients with GCA (1-8). This case illustrates the fact that ischemic optic neuropathy and third cranial nerve palsy may be coincident manifestations of GCA.
Çağatay Öncel, MD
Neurology Department Pamukkale University Denizli, Turkey
Ferda Bir, MD
Pathology Department Pamukkale University Denizli, Turkey
L. Sinan Bir, MD
Neurology Department Pamukkale University Denizli, Turkey email@example.com
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