Neurology India, Vol. 52, No. 3, July-September, 2004, pp. 397-398
Letter To Editor
Giant cell arteritis as a cause of jaw claudication
Yadav Sarita, Bambery Pradeep, Wanchu Ajay, Kakkar Nandita, Singh Surjit
Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012
Correspondence Address:Department of Internal Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh - 160012
Code Number: ni04135
A 65-year-old housewife was admitted with a history of low-grade pyrexia for 10 weeks. A few days later she started having moderately severe throbbing headache, which was more marked on the right side and was especially in the temporal and occipital regions. In addition, she had jaw claudication, which gradually increased in intensity. All peripheral pulsations were normal except for the right temporal artery which was not palpable and the left temporal artery was feeble. The facial artery on right side was cord-like and no pulsations could be felt. Systemic examination was normal. Temporal artery biopsy (right side) revealed intimal proliferation with medial hypertrophy. Elastic lamini revealed disruption. There was moderate chronic inflammatory infiltrate with a few giant cells [Figure - 1] and [Figure - 2]. The patient was treated with steroids (prednisolone -0.3 mg/kg/body wt.) to which she responded rapidly with disappearance of both headache and fever. Steroids were continued on the same dose for a month after which the dose was tapered.
Giant cell arteritis also known as temporal arteritis is a chronic vasculitis of medium and large-sized arteries. It usually involves the cranial branches of the arteries arising from the aortic arch. It generally manifests as fever of low grade and headache, especially over the temporal and occipital areas. On physical examination the frontal and parietal branches of the superficial temporal artery are tender, thickened, nodular or may be absent. Jaw claudication occurs in half of the cases. The other manifestations are partial or permanent loss of vision, mononeuritis multiplex, peripheral neuropathy and strokes involving the territory of the affected artery.
Laboratory investigations usually reveal elevated ESR and C-reactive protein, anemia, generally normocytic normochromic, thromocytosis and decreased serum albumin. Liver enzymes may be elevated. Temporal artery biopsy is diagnostic. The response to corticosteroids is usually rapid. However, 30-50% patients have spontaneous exacerbations and may re quire cytotoxic agents like methotrexate.
Copyright 2004 - Neurology India
The following images related to this document are available:
Photo images[ni04135f2.jpg] [ni04135f1.jpg]