Transoral carotid ultrasonography is useful for detection and follow-up of extracranial internal carotid artery dissecting aneurysm.

Case Report A 62-year-old man having a history of lacunar infarction in the left putamen 4 years previously was referred to a regional hospital with severe headache of sudden onset (day 0). He happened to have had brain magnetic resonance angiography 10 months before, which showed no abnormalities. He had a history of no cardiovascular diseases, hypertension, hyperlipidemia and cervical and cranial trauma. There was no family history of cardiovascular diseases. He was almost normal on general physical and neurological examinations. Although diffusion-weighted magnetic resonance imaging showed no acute ischemic lesions in the brain, magnetic resonance angiography showed the complete disappearance of the right internal carotid artery (ICA). On carotid angiography (CAG), luminal irregularity, severe stenosis and aneurysmal form were found at the C 1 vertebral level of the right ICA. He was transferred to our hospital, and conventional carotid ultrasonography was performed on day 29, which, however, did not find any difference in the diameter and the end-diastolic flow velocities between bilateral common carotid arteries (right 30.3 cm/s, left 31.7 cm/s). The right CAG performed on day 32 showed the persistence of luminal stenosis and aneurysm-like dilatation, with mild improvement of the stenosis ( fig. 1 a). On the same day, TOCU was first performed after informed consent. We used Sonosite Titan version C 2.2 (Sonosite Inc., Bothell, Wash., USA) equipped with an 8to 5-MHz convex array transducer (C8/8–5 MHz) [2] . The transducer was originally designed for prostate imaging and was equipped with a color power Doppler imaging system. The probe tip was painted with echo jelly, covered with a clean cover and softly attached to the posterolateral pharyngeal wall. The attachment of the probe tip to the pharyngeal wall was confirmed by roentgenograms ( fig. 1 b). TOCU clearly demonstrated the dilatation of the right ICA (diameters: right, 8.2 mm; left, 4.0 mm) with narrowing of the true lumen (3.3 mm; fig. 1 c). The aneurysm sac observed on CAG was shown as a protrusion toward the ventral side (the whole length, 2.5 mm; intimal tear length, 7.3 mm). In the false lumen, the isoechoic area indicating intramural hematoma was present around the aneurysm sac, of which thickness was 2.6 mm from the brim of the aneurysm sac to the arterial adventitia. A severe stenotic flow pattern was observed at the distal part of the aneurysm sac (peak systolic flow velocity: right, 232.6 cm/s; left, 120 cm/s). The peak systolic flow velocity ratio (right ICA/ left ICA) was increased to 1.98. On magnetic resonance angiography performed on the same day, the size of the ICA was larger on the right and axial source imaging of time of flight depicted the double lumen in the right ICA: one lumen was hyperintense, indicating blood flow, whereas the other was isointense, indicating intramural hematoma in the false lumen ( fig. 1 d). The false lumen protruded toward the pharyngeal wall. All these findings suggested a diagnosis of spontaneous EICAD. He was treated with long-term antiplatelet (aspirin) therapy. TOCU was performed once a month thereafter, which confirmed the gradual improvement of the narrowing of the true lumen and the decrease in size of both intramural hematoma and aneurysm sac. The peak systolic f low velocity at the distal portion of the right ICA also decreased to that of the left ICA on day 118 (right 92.6 cm/s; left 97.4 cm/s; f low velocity ratio 0.95). On day 245, the protrusion and intimal tear of the aneurysm sac were found to decrease to 1.7 and 5.8 mm, respectively ( fig.1 e). Intramural hematoma, which had been seen at the ventral side of the affected ICA on the first TOCU, was seen at its dorsal side. At the follow-up after 10 months, the patient displayed neither ischemic events nor iatrogenic adverse effects, but mild headache still remained.