Cardioembolism: a rare cause of jaw claudication.

Jaw claudication (JC) results from ischemia of the masticatory muscles, typically caused by temporal arteritis1 and other arteriopathies affecting the external carotid artery (ECA).2,3 We documented a case of JC resulting from cardioembolic occlusion of the ECA and searched both English and French literature on the Medline database (1966-October 2006) to identify previous reports. We combined the keywords “jaw claudication” with either “cardiogenic embolism”, “cardiac embolism”, “cardioembolism”, “etiology”, “cause”, or “carotid occlusion”. A 77-year-old, right-handed man with chronic atrial fibrillation discontinued his oral anticoagulant and underwent toe surgery. Four days later, he experienced new-onset, rightsided jaw pain which was repeatedly provoked by mastication while eating breakfast. This pain did not recur at the next meals. Seven hours after breakfast, he suddenly developed left-sided homonymous hemianopia, paresis, hypoesthesia, and spatial neglect. He denied previous neurological symptoms, shoulder pain or stiffness, and constitutional symptoms. On palpation, his temporal arteries were painless, non-nodular, and pulsated normally. His temporomandibular joints were unremarkable. No carotid artery or cardiac murmurs were detected. Brain CT showed a subacute right middle cerebral artery infarct. Ultrasonography of the right ECA failed to reveal a patent lumen at grey-scale B-mode scanning and demonstrated absence of flow at spectral, power and color Doppler imaging techniques, consistent with total occlusion.4 The left ECA was normal. Bilateral internal carotid artery stenoses of ≤20% were present. An EKG confirmed atrial fibrillation. Echocardiography did not reveal other sources of embolism or thrombus. C-reactive protein (CRP) was 7.0 mg/L (normal ≤5.0). Erythrocyte sedimentation rate (ESR) and levels of white blood cells, hemoglobin, platelets, and fibrinogen were normal. We diagnosed JC resulting from cardioembolic occlusion of the right ECA and cardioembolic stroke. Anticoagulant therapy was reinitiated one week after presentation. This individual did not receive anti-inflammatory or immunosuppressive drugs. Three months after stroke, his CRP had decreased to 5.15 mg/L. Repeat ultrasonography by the same operator revealed normal temporal and external carotid arteries, including a re-canalized right ECA without residual stenosis. This individual experienced no additional symptoms during a clinical follow-up of 24 months. He remains with hemianopia, mild hypoesthesia and sensory neglect on the left side. Cardioembolism: A Rare Cause of Jaw Claudication