An 83-year-old sedentary man with hypertension, hypercholesterolemia, coronary insufficiency, and diabetes mellitus presented with an acute transient sensory right hand deficit while eating, without pain. There was no recent head or cervical trauma. Clinical examination was normal. Brain MRI showed a chronic (asymptomatic) watershed infarction between the left posterior and middle cerebral arteries, and no recent infarction. A diagnosis of a transient ischemic attack was made. Because of the co-existence of a chronic left-sided watershed infarction, an underlying left carotid artery pathology was suspected. Carotid duplex examination showed a large atheromatous plaque at the proximal internal carotid artery (ICA) with an irregular surface, associated with a 50% stenosis. Velocities did not change after head rotation. CT angiography confirmed focal vasculopathy (and the 50% stenosis) in the anteromedial side of the ICA, in near contact with the left-sided greater horn of the hyoid bone (Figs. 1, 2). Fat-saturation T1/T2 MRI, in search for ICA dissection, did not show intramural hematoma or ICA dilatation. Suspecting an artery-to-artery embolism, heparin treatment was given for 1 week, followed by oral anticoagulation, which was switched to acetylsalicylic acid after 3 months. Because of the patient’s age and associated co-morbidities, surgery (partial hyoid bone resection) was not performed. Rare cases of hyoid bone-related focal carotid pathology have been reported [1–5]. Two patients had a carotid pseudoaneurysm (probably related to earlier dissection), and three patients had a (non-atherosclerotic or atherosclerotic) vasculopathy (2 with a moderate and 1 with a 90% stenosis) explained by mechanical ICA compression. In two of these earlier reported patients, repetitive trauma seemed to play a role (playing golf, and carrying heavy weight on the shoulder) in the pathogenesis. Surgical partial hyoid bone resection has been performed in some of the earlier described patients without complications. Possible etiologies in hyoid bone-related carotid pathology include dissection, pseudoaneurysm, stenosis, or occlusion due to direct compression, and pressure-induced plaque formation (directly by hyoid bone compression leading to constructional changes in the carotid wall contour or indirectly by changes in blood flow and shear forces) and/or rupture. Each of these causes may potentially lead to stenosis, occlusion, or artery-to-artery embolism. Our patient had no high grade stenosis, no arguments on duplex examination for intermittent head position-related stenosis, and no excessive head rotation or external compression. Our patient had a sedentary lifestyle due to coronary insufficiency and no arguments in favor of ICA dissection. Repetitive head rotation in normal daily life (associated with mild carotid compression by the hyoid bone) seemed to have led to the formation of an atheromatous plaque and potentially also for mechanical plaque rupture, leading to artery-to-artery embolism. D. Renard (&) P. Labauge Department of Neurology, CHU Nimes, Hopital Caremeau, Place du Pr Debre, 30029 Nimes Cedex 4, France e-mail: dimitrirenard@hotmail.com