A reconstruction of the<unk>  arteries from a CT scan, seen from the front. From the bottom, V1 is from the subclavian artery to the foramina, V2 is from the foramina to the second<unk>  V3 is between the foramina until entry into the skull, and V4 is inside the skull embedded in the dura mater. They merge into the basilar artery, which then divides into the posterior cerebral artery. The<unk>  arteries arise from the subclavian artery, and run through the transverse foramen of the upper six<unk>  of the neck. After exiting at the level of the first cervical<unk>  its course changes from vertical to horizontal, and then enters the skull through the foramen magnum. Inside the skull, the arteries merge to form the basilar artery, which joins the circle of Willis. In total, three quarters of the artery are outside the skull; it has a high mobility in this area due to rotational movement in the neck and is therefore vulnerable to trauma. Most<unk> s happen at the level of the first and second<unk> . The<unk>  artery supplies a number of vital structures in the posterior cranial fossa, such as the brainstem, the cerebellum and the occipital lobes. The brainstem harbors a number of vital functions (such as respiration) and controls the nerves of the face and neck. The cerebellum is part of the diffuse system that coordinates movement. Finally, the occipital lobes participate in the sense of vision.<unk>  occurs when blood accumulates in the wall of the blood vessel. This is most likely due to a tear in the tunica intima (the inner layer), allowing blood to enter the tunica media, although other lines of evidence have suggested that the blood may instead arise from the vasa vasorum, the small blood vessels that supply the outer layer of larger blood vessels. Various theories exist as to whether people who sustain carotid and<unk> , even if not suffering from a connective tissue disorder, have an underlying vulnerability. Biopsy samples of skin and other arteries has indicated that this might be a possibility, but no genetic defect in collagen or elastin genes has been convincingly proven. Other studies have indicated inflammation of the blood vessels, as measured by highly sensitive C-reactive protein (hsCRP, a marker of inflammation) in the blood. Once<unk>  has occurred, two mechanisms contribute to the development of stroke symptoms. Firstly, the flow through the blood vessel may be disrupted due to the accumulation of blood under the vessel wall, leading to ischemia (insufficient blood supply). Secondly, irregularities in the vessel wall and turbulence increase the risk of thrombosis (the formation of blood clots) and embolism (migration) of these clots of the brain. From various lines of evidence, it appears that thrombosis and embolism is the predominant problem. Subarachnoid hemorrhage due to arterial rupture typically occurs if the<unk>  extends into the V4 section of the artery. This may be explained by the fact that the arterial wall is thinner and lacks a number of structural supports in this section.
Vertebral artery dissection
Cervical artery dissection
Carotid artery dissection
Posterior cerebral artery syndrome
Middle cerebral artery syndrome
Anterior cerebral artery syndrome
ROSAH syndrome
Pseudosubarachnoid hemorrhage