Its pathogenesis is believed to be associated with trauma, but it has also been reported as an unusual form of organized thrombus [6], [7], [8] and [9]. A 43 years old female with neither previous history of neurological diseases nor vascular risk factors other than smoking custom, was admitted to our Neurological Department – Stroke Unit, because of a left hemiparesis. She had felt her left arm somehow weak, strangely “cold”, in the previous afternoon, but believing that

this was related Lenvatinib mouse to fatigue she went to sleep. On admission a mild left sided sensorimotor hemiparesis was found with a NIHSS of 8. The brain CT scan performed at the admission showed a “dot Dabrafenib molecular weight sign” in a M2 branch of the right Middle Cerebral Artery (MCA) (Fig. 1) and a right fronto-parietal ischemic stroke (PACI) (Fig. 2). The EC US revealed at the origin of the internal carotid artery, an hyperechogenic lesion (Figs. S1 and S2). It was somehow different

from an atherosclerotic plaque and more similar to a soft tissue mass. Its echogenicity was homogenous and, in its distal portion, it was partially separated from the arterial wall, but no flapping movement was evident (video). The lesion occupied more than 75% of the cross sectional area of the vessel, but no increased velocity was present (Figs. S3, and 3). At TCCD Celecoxib all the major intracranial arteries were insonated; an asymmetry of the MCA velocities (R < L), with a Zanette index of 26.39 suspicious for a right MCA distal occlusion, was found (Figs. S4 and S5). The Angio-CT confirmed these features (Figure 4 and Figure 5). The patient was evaluated for vascular risk factors, dietary factors (Folate, B12), and methylene tetra hydro folate reductase (MTHFR) polymorphism;

a thrombophilic screening was also performed. The condition of homozygosis for MTHFR was present. The histological diagnosis was consistent with a diagnosis of IPEH (Fig. 6): a marginal endothelial papillary hyperplasia, surrounding a fibrous and hematic material like an organized thrombotic formation, was described. From the therapeutical point of view an antiplatelet therapy was started at the admission and the following days the clinical condition progressively improved. The vascular surgeon was then consulted and a surgical procedure was performed to remove the lesion. When dismissed the patient was asymptomatic, the NIHSS equal to 0 and she did not suffer from any other symptom during the following 2 years. The EC US (Figs. S6 and S7), 2 years later, revealed some hyperplasia at the origin of the ICA possibly representing the over-expression of the post-CEA neoendothelial growth or the evolution of the incompletely removed lesion and showed that a longer follow-up is necessary.