Scientists/radiologists who study brainstem injuries and cerebrovascular diseases.Bilateral damage to the rostral brainstem causes coma by disrupting the ascending pathways of the reticular activating system^1,2. Despite the relevance of coma-causing brainstem lesions to multiple human diseases, an animal model of coma due to brainstem injury is lacking. Here, we attempt to induce a comatose state in a rat by producing a focal brainstem infarction. We occluded the basilar artery (BA), which is the primary source of blood supply to the rostral brainstem, at two points³, sparing the anterior inferior cerebellar artery (AICA). We first mapped the neuroanatomical distribution of the resulting brainstem infarction. Using a high resolution MRA method, we then mapped the major branches of the BA. The two-point BA occlusion reproducibly produced infarction of medial and ventral brainstem, but the rats were not comatose. This result provides a foundation to further modify the BA occlusion strategy to more precisely target the arousal pathways of the reticular activating system and induce a comatose state in rats.For BA occlusion, the anesthetized animals were secured dorsally and the cervical skin was shaved and cleaned with 10% povidine iodine. After dissecting the sternohyoid and omohyoid muscles, the base of the occipital cranium was exposed. A high speed drill was used to thin the exposed basilar bone and the dura was opened widely. The BA and several branches could be identified (Fig. 2 A) and two points along the BA were permanently occluded with 6-0 silk suture (Fig. 2 B). An MRI scanner with a 14T magnet (Agilent, with a Bruker Biospin AVIII console system) equipped with a 12 cm gradient set, capable of providing 100 G/cm with a rise time of 150 ms was used for the characterization of the brain of healthy and BA-occluded rats. A FLASH sequence was used to visualize vasculature in the brain (MR Angiography), setting an Echo Time (TE) of 1,867 ms and a Repetition Time (TR) of 20 ms with flip angle at 50°, which allows highlighting the blood vessels (Fig.1 and Fig.2 B). For T2-weighted images that allow detection of infarcted areas (visualized as bright zones), a RARE sequence was used, with TE = 35.88 and TR = 2000 ms (Fig. 2 C-F).Nerve tissue in brainstem is supported by a capillary network emerging from two vertebral arteries, which join to form the BA. Small branches of the BA penetrate deeper into the brainstem, which was detected with the high resolution MRA sequence (Fig 1). Large arteries travelling over the ventral brainstem are readily observable through craniotomy in the ventral skull in vivo (Fig. 2 A), and a picture of the whole network can be realized with short-TR MR sequences (MRA, Fig. 1 and Fig. 2 B). BA occlusion above the level of AICA (Fig. 2 B) resulted in vanishing of the corresponding BA segment when visualized with MRA (data not shown). Disruption of blood flow within the BA triggered the emergence of infarcted areas in the medial-ventral brainstem, which could be detected with T2-weighted MRI (Fig. 2 C and E, compared to Fig. 2 D and F). Nevertheless, BA-occluded rats did not enter a comatose state, and thus a large-scale constriction affecting AICA (besides BA) to occlude blood to the dorsal brainstem might be used in future studies intended to induce an unarousable state.High resolution MRA was used to characterize the main vessels that supply blood to brainstem, showing the BA and numerous branches that penetrate deeper through the medulla, pons and part of the midbrain. Occlusion of BA resulted in local blood flow disruption confirmed by MRA and subsequent infarcts to the brainstem observed in T2-weighted images, setting the base for the development of a model for local injury to brainstem in the rat.