7 Among TIA presentations, limb-shaking TIAs are peculiar transient symptoms frequently associated with high-grade stenosis, often in the ICA. The natural history of patients with ICAD comprises 3 predominant courses that may coexist: transient ischemic attack (TIA), recurrent ischemic stroke, and chronic hypoperfusion that can cause cumulative white matter damage and gradual cognitive worsening. 8,9 Mixed patterns are common (eg, high-grade stenosis causing border zone and embolic patterns) and may be caused by endothelial abnormalities from ICAD inducing clot formation and distal embolization, compounded by hypoperfusion preventing appropriate washout of emboli in the border zones.
Atheromatous encroachment on the opening or ostia of small perforators causing occlusion results in a subcortical perforating pattern of infarct (branch atheromatous disease), with infarcts usually less than 1.5 cm. 8 Another mechanism, hypoperfusion distal to the stenotic artery, causes border zone infarcts either in the internal border zone comprising the corona radiata and centrum semiovale or in the cortical border zones between the anterior cerebral artery (ACA), middle cerebral artery (MCA), or MCA-posterior cerebral artery (PCA) vascular territories. 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).