Thrombosis The origin of the internal carotid artery is the most common site for the development of atherosclerotic stenosis; in addition, the siphon segment of the ICA (internal carotid artery) is a favored site for atheromatous plaque, whereas other parts of the ICA are rarely involved. Compared with the extracranial and siphon segments of the ICA, atherosclerotic thrombosis was less likely to occur in the anterior supratentorial segment of the ICA, the trunk of the MCA (middle cerebral artery), and the trunk of the ACA (anterior cerebral artery) in whites. However, in black, Chinese, and Japanese populations, the incidence of MCA lesions was higher than that of ICA lesions. Figure 1 Preferred sites of atherosclerotic stenosis: plaques are indicated in gray. In the posterior circulation, the beginning of the vertebral and subclavian arteries, the proximal and distal ends of the intracranial segment of the vertebral artery, the proximal and distal ends of the basilar artery, and the beginning of the posterior cerebral artery are the preferred sites of atherosclerotic stenosis. Figure 1 shows the common sites of atherosclerosis. Atherosclerotic stenosis rarely involves the cerebral arteries (ACA, MCA, PCA) and the distal superficial branches of the cerebellar arteries (PICA, AICA, SCA). Figure 2 Coronal view of the cerebral hemisphere showing the main trunk of the middle cerebral artery and its branches, the ductus arteriosus. The lipohyalinosis and mesenteric hyperplasia caused by hypertension mainly involve: (1) the penetrating branches of the ductus arteriosus of the middle cerebral artery (Figure 2); (2) the penetrating branches of the anterior cerebral artery, usually the Heubner artery (Figures 3 and 4); (3) the penetrating branches of the anterior communicating arteries (Figure 5 and Figure 3); (iv) thalamic penetrating arteries and thalamic geniculate penetrating branches from the posterior cerebral arteries (Figure 3); and (v) paracentral penetrating branches from the basilar arteries that reach the pons, midbrain, and thalamus. In some cases, atherosclerotic plaque formation in the parent artery or microscopic atherosclerotic plaque at the mouth of the penetrating branch can block the penetrating artery (Figure 6). The sites of involvement of atherosclerotic feedthrough occlusions are the same as in lipohyalinosis, but also the former can involve larger arteries (e.g., the anterior choroidal artery, a branch of the internal carotid artery, and the thalamic geniculate artery, which emanates from the posterior cerebral artery). Figure 3 Penetrating arteries of the basal ganglia and thalamus Figure 4 Coronal post-mortem angiogram showing branches of the anterior cerebral artery (white arrow). The area of black dots (left side of the image) is the internal junctional area. (From Pullicino P: Lenticulostriate arteries. In Bogousslavsky J, Caplan LR (eds): Stroke Syndromes, 2nd ed. Cambridge: Cambridge University Press. 2001, pp 428-437.) Figure 5 Extent of blood supply to the anterior choroidal artery Figure 6 Pathological manifestations of atherosclerotic penetrating lesions: (A) plaque in the parent artery occluding the entrance of the penetrating branch; (B) plaque in the parent artery extending into the penetrating branch; (C) microscopic atherosclerosis at the entrance of the penetrating branch. The most common sites of arterial entrapment due to traumatic or spontaneous vessel wall tears include the pharynx of the carotid artery, the portion of the vertebral artery from its origin to just before it enters the intervertebral foramen, and the V3 segment of the vertebral artery (the portion of the cervical spine that coils around the side of the mouth to just before it crosses the dura into the cranial cavity). At these sites, the carotid arteries are not dependent on other arteries or bony structures and are therefore relatively more mobile. The most common cause of carotid artery wall tears is sudden strain on the artery or direct trauma. In addition to the common sites of entrapment described above, other less common sites of entrapment formation include the intracranial segments of the ICA, MCA, and VA, as well as the basilar artery. Temporal arteritis most often involves the portion of the ICA and VA that is about to cross the dura into the skull, as well as the anterior branch of the ophthalmic artery into the brain. Embolism Emboli of different sizes, properties, and origins can occlude different arteries. Larger emboli (usually of cardiac origin) can sometimes embolize large extracranial arteries, such as the cephalobrachial trunk, subclavian artery, carotid artery and vertebral artery in the neck. Smaller emboli formed in cardiac or peripheral arteries often embolize intracranial arteries, such as the ICA, ACA, VA basilar artery, PCA, and MCA, with embolization of the main trunk of the MCA or its superior or inferior trunks being the most common. In the anterior circulation, the most common site of embolization is the MCA and its branches. Animal studies have shown that microscopic foreign bodies released into the ICA can enter the branches of the MCA along the blood flow. In the posterior circulation, the most common sites of embolism are the intracranial segment of the VA, the basilar artery, and the PCA. In addition, microscopic emboli, such as thrombus fragments, platelet-fibrin aggregates, biliary homogeneous alcohol crystals or other debris from lipid plaques, and calcified debris from heart valves or arterial walls, can embolize small penetrating arteries of the brain or cerebellum, ophthalmic arteries, and retinal arteries. Cerebral hemorrhage Figure 7 Horizontal section of the brain and sagittal plane of the brainstem, showing common sites of cerebral hemorrhage. The most common cause of cerebral hemorrhage is {blood pressure at the same site as hypertensive arterial lipohyalinosis (Figure 7).The concept of microaneurysm was first introduced by Charcot and Bouchard in 1872, who suggested that cerebral hemorrhage was caused by rupture of a microaneurysm. Even if the patient does not have a long history of hypertension, the sudden increase in blood pressure and cerebral blood flow can cause rupture of the above-mentioned penetrating artery, which can lead to cerebral hemorrhage. In contrast, cerebrovascular malformations can cause cerebral hemorrhage at any site; in addition, cerebral amyloid angiopathy involving the subarachnoid space and small and medium-sized arteries and microarteries within the cerebral cortex is also a cause of cerebral hemorrhage. Figure 8 The most common sites of intracranial aneurysms: (a) PICA; (b) basilar artery; (c) PCoA; (d) ICA; (e) ACoA; (f) MCA bifurcation. Subarachnoid hemorrhage The common site of aneurysm is the junction of the major arteries that make up the Willis ring. The most common sites are the ICA-PCoA junction, the ACoA-ACA junction, and the MCA bifurcation; in addition, the supratentorial segment of the ICA, the pericallosal artery, the VA-PICA junction, and the tip of the basilar artery are also good sites for aneurysms (Figure 8). Arteriovenous malformations causing subarachnoid hemorrhage are often located in the brain parenchyma near the surface of the soft meninges or ventricles, in the ventricular system, or in the subarachnoid space; some large arteriovenous malformations are sometimes located entirely in the subarachnoid space.