Intermittent Claudication of the Jaw
A 56-year-old white male presented with syncope and a history of ventricular premature contractions. His symptoms were preceded by dizziness, which had been a recurrent problem over the past year. These episodes were brief, each lasting less than 1 minute. He recovered completely and did not suffer any injuries.
The patient’s Cestamibi stress test was indeterminate. His echocardiogram showed normal chamber sizes and a 60% EF. We performed a cardiac catheterization and discovered four patent vein grafts that had been placed 36 months prior.
The patient underwent an electrophysiologic study, which did not show inducible supraventricular tachycardia or ventricular tachycardia.
We referred the patient to a neurologist. An EEG scan was negative, but a carotid duplex examination suggested 80% to 99% stenosis in the right internal carotid artery. The neurologist sent the patient back to us for a carotid angiogram and advised that angioplasty as well as stenting might be necessary at the time of the diagnostic study. We enrolled the patient in a research treatment protocol, which required a baseline CT scan of his head and semiannual monitoring by the neurologist. The CT scan did not show any significant pathology.
The great vessels had smooth patency at and beyond their origins off the aortic arch. The left carotid system was unremarkable, and the subclavian/vertebral systems were patent in their proximal portions. Plaque began in the right distal common carotid artery and extended into both the internal (85% stenosis) and external (40% stenosis) carotid origins. Figure 1A shows the right carotid artery.
We performed angioplasty with a 6-mm OPTA V balloon (Cordis Corporation, a Johnson & Johnson Company, Miami, FL) and stenting with a 7-cm X 20-mm self-expanding Smart stent (Cordis Corporation). Our efforts resulted in the completion angiogram shown in Figure 1B.
The balloon and stent procedure was successful regarding patency in the internal carotid artery. However, considerable plaque shift occurred and resulted in a subtotal occlusion of the external carotid artery. This finding is not usually an issue because of the size of this patient’s external carotid artery. When the artery nearly closed acutely, however, the patient developed symptoms of claudication in his right masseter muscle while chewing. These symptoms worsened when he chewed meat and other tough foods and abated completely when he discontinued chewing for 1 minute. He had no neurologic symptoms and at his 6-month follow-up visit, his symptoms were negligible (although they persisted in extreme circumstances). At the patient’s 1-year follow-up visit, his symptoms completely disappeared.
HOW WOULD YOU PROCEED?
1. Would you recommend painkillers? OTC or prescription?
2. Would you make the connection between claudication and stenting?
3. Would you consider checking an erythrocyte sedimentation rate?
Muscle pain while chewing has been widely reported in patients with giant cell arteritis and is considered a key finding in patients with this condition. Polymyalgia rheumatica also can be associated with masticatory muscle pain and is usually seen in patients in their seventh decade.
Our patient’s symptoms had a strong temporal relationship to near-closure of his external carotid artery. Similar to claudication in peripheral skeletal muscles, the masseter muscle is also susceptible to ischemia as identified in this patient.
Poisson et al reported what was believed to be the first case of jaw claudication as a result of extracranial carotid atherosclerosis involving only the external carotid artery.1 Webster et al reported jaw claudication as a result of atherosclerosis in the carotid bifurcation.2 Their patient was initially thought to have giant cell arteritis, but had a negative workup and no response to corticosteroids. Venna et al presented a case in which the patient underwent a similar workup for inflammatory markers, which turned out to be negative.3 Other causes of intermittent claudication of the jaw include Wegener’s granulomatosis, primary amyloidosis, and external carotid ligation for posterior epistaxis.4-6
James A.M. Smith, DO, is Director of Vascular Medicine at the University of Pittsburgh Medical Center in McKeesport, Pennsylvania. Dr. Smith may be reached at (412) 664-2507; email@example.com.
Carol Minnich, RN, BA, is currently employed by Adventist Healthcare Systems in Takoma Park, Maryland. Ms. Minnich may be reached at cminnich@iGlide.net.
Daniel Paolantonio, MD, Adolfo Rodriguez, MD, and Carlos Vozzi, MD, are staff cardiologists at the Institute for Cardiovascular Interventions in Rosario, Argentina. They may each be reached at firstname.lastname@example.org.
1. Poisson M, Mashaly R. Occlusion of external carotid artery causing intermittent claudication of the masseter. Br Med J. 1978;9:1611.
2. Webster G, Beynon, Walport. Jaw claudication and amaurosis fugax secondary to atheromatous disease of the carotid arteries [letter to the editor]. Br J Rheum. 1994;33:691-692.
3. Venna, Nagapopal N, Goldman, et al. Temporal arteritis-like presentation of carotid atherosclerosis. Stroke. 1986;17:325-327.
4. Vermeulen J, Mahow M. A case of Wegener’s granulomatosis presenting with jaw claudication. J Rheum. 1984;11:707-709.
5. Motamed, Farrell M, Philpott. Claudication on mastication following bilateral external carotid ligation for posterior epistaxis. J Laryngol Otol. 1998;112:73-74.
6. Frayha, Abu-Haidar F. Polyarteritis nodosa masquerading as temporal arteritis. J Rheum. 1979;6:76-79.