![]() Artery-to-artery embolism from a ruptured plaque and thrombo-occlusion of the diseased artery are typically associated with a territorial pattern of infarct via occlusion of the stenotic artery or its more distal branches, which produces infarcts that are typically larger than 1.5 cm. ICAD may cause stroke via several different mechanisms, which may be inferred by the pattern of infarct on MRI. 7 At least part of this ethnic difference is thought to come from the higher rate of uncontrolled hypertension, diabetes, and hyperlipidemia in the Asian, Hispanic, and black populations, although genetic predispositions may also exist. 5,6 Asians in particular have a higher burden of ICAD, with one study suggesting it accounts for 33% to 37% of ischemic stroke etiologies in China. Asian, black, and Hispanic populations are more affected than the white population, although the prevalence in this latter group is higher than once commonly thought. ![]() 4 Men have a higher rate of development of ICAD during their fourth and fifth decades, while women generally only begin developing plaque in their sixth decade. Although early-onset disease is well-described in certain populations, clinically meaningful atherosclerotic plaque does not typically appear until the fourth decade of life, and the highest rate of development of significant ICAD is between the sixth and seventh decades. Age, race, and sex are the most typical of the nonmodifiable risk factors. Hypertension, diabetes mellitus, hyperlipidemia, and smoking are the most typical modifiable risk factors. Risk factors for ICAD fall into modifiable and nonmodifiable categories. Here, we briefly discuss the epidemiology and pathophysiology of ICAD and strategies for acute and long-term management. 3 For the practicing neurologist, diagnosing and treating ICAD can be challenging because it can masquerade as and be confused with other conditions and because ICAD is associated with high rates of recurrent stroke. In autopsy studies, ICAD accounted for 10% of strokes, 2 and in a pooled analysis of 2,593 patients, it was at least somewhat present in 3.5% to 13% of the population, varying with age and ethnicity. 1 As such, ICAD is not amenable to surgical revascularization, making it a very different and independently important disease entity from extracranial carotid disease. Intracranial atherosclerotic disease (ICAD) can affect cerebral arteries distal to the internal carotid arteries (ICAs) after they enter the petrosal bone (C2 segment) and the vertebral arteries after they enter the foramen magnum and pierce the dura mater (V4 segment).
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