On FLAIR, there is abnormal high signal intensity in the medial frontal lobe (ACA territory) on the right, involving both gray and white matter, with mild mass effect upon the frontal horn of the lateral ventricle. 1.57 Anterior cerebral artery (ACA) infarct, early subacute. There is also hemorrhage ( black arrow) within the lesion, seen with low signal intensity due to a T2* effect. In this instance, infarcts of the same time frame are also seen in the left thalamus ( white arrow), which is supplied by the posterior thalamoperforators (which originate from the P1 segment of the PCA). There is both vasogenic edema and cytotoxic edema, as demonstrated by respectively high signal intensity on the T2- and the diffusion-weighted scans, in the entirety of the left PCA distribution. 1.56 Posterior cerebral artery (PCA) infarction, early subacute. The ACA supplies the anterior putamen, caudate nucleus, hypothalamus, corpus callosum, and medial surface of the cerebral hemisphere ( Fig. The PCA supplies the posteroinferior temporal lobe, medial parietal lobe, occipital lobe, and portions of the brainstem, thalamus, and internal capsule ( Fig. The PCA can originate from the tip of the basilar artery (80%) or in the case of a fetal origin (20%) directly from the internal carotid artery. The MCA supplies the lateral cerebral hemispheres, with the lenticulostriate arteries (arising from the M1 segment) supplying the globus pallidus and putamen and the anterior limb of the internal capsule. Of the three major arterial territories, ACA infarcts are by far the least common. MCA infarcts are most common, followed by PCA infarcts. Infarcts in the major arterial territories are easily recognized due to their arterial distribution and their involvement of both gray and white matter. The latter two statements apply to patients who are left-hemisphere dominant. Infarction in the left posterior superior temporal gyrus (specifically in Wernicke′s area) causes receptive aphasia. Infarction in the left inferior frontal gyrus (specifically in Broca′s area, the part of the brain responsible for speech production) causes an expressive aphasia. Infarction involving the precentral gyrus (primary motor cortex) leads to contralateral motor deficits. The clinical presentation is that of an acute neurologic deficit. Risk factors for infarction in an adult include high blood pressure, high cholesterol, smoking, diabetes, obesity, cardiovascular disease, oral contraceptives, and cocaine. Following mechanical thrombectomy (3 hours following the CT), flow to the left MCA and its branches was fully restored (image not shown).Ĭommon areas of atherosclerotic involvement include the carotid bifurcation, distal internal carotid artery, and middle cerebral artery. The occlusion ( black arrow) was confirmed on DSA. CTA reveals thromboembolic occlusion ( white arrow) of the distal left M1 segment of the MCA. The time to peak (TTP) image reveals delayed perfusion in nearly the entire left MCA territory, with the exception of the lenticulostriate artery distribution. The unenhanced CT (not shown) was grossly unremarkable. This 79-year-old woman presented 1.5 hours prior to the initial imaging evaluation with clinical signs of ischemia in the left MCA territory. 1.55 Hyperacute distal MCA territory infarct, evaluation by CT. In the elderly, infarcts are most often due to atherosclerosis, with vessel occlusion due to either thrombosis or embolism ( Fig. Leading causes include congenital and acquired heart disease, together with sickle cell disease. In young patients, the etiologies for cerebral infarction are many and varied, in distinction to adults.

Pica infarct