Carotid artery perforation

The posterior cerebral artery encircles the midbrain close to the oculomotor nerve at the level of the tentorium and supplies the inferior part of the temporal lobe, and the occipital lobe (Marinkovic et al. 1987). Many small perforating arteries arise from the proximal portion of the posterior cerebral artery to supply the midbrain, thalamus, hypothalamus and geniculate bodies. Sometimes a single perforating artery supplies the medial part of each thalamus, or both sides of the midbrain. In approximately 15% of individuals, the posterior cerebral artery is a direct continuation of the posterior commrmicating artery, its main blood supply then coming from the internal carotid artery rather than the basilar artery. 

In Japanese, moyamoya means puff of smoke and describes the characteristic radiological appearance of the fine anastomotic collaterals that develop from the perforating and pial arteries at the base of the brain, the orbital and ethmoidal branches of the external carotid artery and the leptomeningeal and transdural vessels in response to severe stenosis or occlusion of one, or both, distal internal carotid arteries (Yonekawa and Khan 2003). The circle of Willis and the proximal cerebral and basilar arteries may also be involved. 

Ischemic strokes account for around 80-85% of all strokes and are caused by arterial vascular occlusions rarely occlusion in the cerebral venous system may result in ischemic and/or hemorrhagic stroke. Arterial occlusions resulting from cerebral embolism are the most common causes of ischemic strokes, and by about one week after stroke as many as 70-90% of occlusions will have spontaneously recanalized. Emboli typically originate from atherosclerotic stenoses in the internal carotid artery or from sources in the heart such as clots in the left atrium or the left ventricle. Hypertension-induced vascular disease of the small perforating intracerebral arteries is a common cause of lacunar strokes. A classification of the major stroke subtypes is shown in Table 31.1. 

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